A Review of the Ingested Fluoride
by Mark D. Gold
Scientific Risk Assessment Symposium
by Jeff Green
On June 19-21, 1998, concerned citizens, physicians, dentists, nurses, and
water department officials gathered from 11 states, Canada, and northern
and southern California to attend a symposium held in San Diego,
California entitled "Drinking Water Fluoridation & Ingested Fluoride - -
Scientific Risk Assessment."
The symposium focused on the processes and relevant science that contribute
to the establishment of a Public Health Goal (PHG) for fluoride in
accordance with the California Safe Drinking Water Act of 1996
(adopted from the U.S. Safe Drinking Water Act of 1996).
The California Environmental Protection Agency's Office of
Environmental Health Hazard Assessment (OEHHA) is required to
establish PHGs for acutely toxic substances at levels at which
scientific evidence indicates that no known or anticipated adverse
effects on health will occur over a lifetime of exposure, plus an
PHGs are to be based solely on scientific and public health
considerations, without regard to economic considerations, and
exert no regulatory burden or mandatory goals. PHG documents are
developed for technical assistance to Department of Health Services
and may also benefit federal, state, and local public health
officials. In effect they are to be the scientific bases for public
David Morry, Ph.D, Staff Toxicologist, OEHHA, author of the December
1997 Public Health Goal for Fluoride in Drinking Water, began the
symposium by defining the newly mandated criteria for evaluating
contaminants in the drinking water, and his specific methodology
and determinations in setting a PHG for fluoride of 1 mg/L.
The PHG adopted by the OEHHA was based on a no-observed-adverse-effect
level (NOAEL) of 1 mg/L for dental fluorosis in children, with a
relative source contribution (percentage of drinking water contribution
to total intake of fluoride from all sources) of 100% and an
uncertainty factor (margin-of-safety) of 1.
Throughout his presentation, questions from the audience, and panel
discussions, Dr. Morry characterized the PHG for fluoride as an
ongoing process and was candid and precise in identifying the materials
he reviewed, and the materials he was not aware of, in reaching his
Dr. Morry described that consideration of beneficial effects is rare
in establishing toxicological assessments and, had he not weighted a
dental benefit from ingested fluoride in his considerations, he would
have applied an uncertainty factor that would have altered the PHG
to 0.1 to 0.3 mg/L.
Other factors identified by the audience, other speakers, or his own
review, that Dr. Morry warranted deserving of further consideration:
Sources for determination of dental benefit were limited to two
review documents from the Public Health Service and the National
Research Council, and discussions with Dr. Robert Isman and
Dr. Howard Pollick, known fluoridation proponents. No in-depth
inspection of scientific literature concerning dental
benefit was performed. No attempt was made to quantify a dental
Phyllis Mullenix, Ph.D., co-founder of the first toxicology laboratory
for dentistry in the nation at Forsyth Dental Research Institute
(an affiliate of Harvard), and now of Children's Hospital, Boston,
MA. outlined a history of twenty-seven studies addressing fluoride's
effect on the brain and neurological behavior, dating back to 1869.
Dr. Mullenix provided references to the science that she states
should have been sufficient warning to reduce further exposure
until comprehensive studies could be performed to ascertain the
true extent of effects.
While the total intake assessment used by the OEHHA included other
sources of fluoride, ranging from 1.1 to 4.6 mg/day for children
in fluoridated communities and 1.9 to 7.0 mg/day for adults, the
adopted PHG assumed that all epidemiological studies reviewed
with 1 ppm in the water represented the same total intake.
The OEHHA did not attempt to make an adjustment for different
levels of total intake for studies that identified water
concentration at 1 ppm, yet obviously represented a lower level
of total exposure; such as the studies of the incidence of dental
fluorosis performed before fluoride appeared in toothpaste and
mouth rinse, as well as in Classic Coke, Gerber's baby juices,
Fruit Loops, pharmaceuticals and virtually every other food and
beverage processed with fluoridated water or exposed to
Review materials did not include the corrected version of a
second animal study which revealed additional osteosarcomas
that, coupled with higher incidence of osteosarcoma in human
populations, may elevate carcinogenicity as an end-point for
fluoride risk assessment.
Review materials did not include recent studies (1994-present),
including those linking hip fracture, kidney damage, or
neurological impairment to low levels of fluoride exposure.
Dr. Mullenix described her behavioral study (Neurotoxicology
and Teratology, Vol.17, no. 2 pp. 169-177,1995) depicting
hyperactivity and hypoactivity in laboratory animals as a result
of prenatal and postnatal exposure to fluoride; clarifying the
conditions of the study, dose-exposure vs plasma levels, behavioral
response consistency with other studies, fluoride accumulation in
the brain, and prenatal exposure timing with respect to brain
Dr. Mullenix offered specific potential mechanisms for fluoride's
effects on the brain, including inhibition of cell proliferation,
delay of cell differentiation, antimetabolite properties,
increased cAMP, interaction with Ca, Mg, Al, anticholinesterase
activity, and enhancing activity such as penetration into the brain.
Dr. Mullenix provided personalized insight into the institutionalized
political interference that has inhibited the pursuit of science to
resolve the still-unanswered questions.
Lennart Krook, D.V.M., Professor of Pathology, Emeritus, College
of Veterinary Medicine, Cornell University, and author of more than
200 scientific papers, provided precise images and explanations of
the physiological mechanisms of bone pathologies, dental fluorosis
and reproductive toxicity found in cows and other animals effected
by exposure to fluoride.
Dr. Krook expressed that the normal mineral phase of hard tissues
is calciumhydroxyapatite, and that when fluoride is available,
fluoride replaces the hydroxyl ions, and calciumfluoroapatite is
built in. This is toxic to the cells forming and retained in the
respective hard tissues, viz. osteoblasts and osteocytes, ameloblasts
and odontoblasts, and cementoblasts and cementocytes.
Dr. Krook presented the audience and panel with graphic insight
into dose-weight correlation and the devastating effects of fluoride
Karl Jensen, Ph.D., Neurotoxicological Division, National Health
and Environmental Effects Research Laboratory, US EPA, Research
Triangle Park, NC. reviewed the findings of the study he recently
co-authored (Varner et al., Brain Research, 784: 284-298, 1998).
Dr. Jensen described alterations in neuronal and cerebrovascular
integrity, similar to that found in humans with Alzheimer's and
other forms of dementia, when laboratory rats were chronically
exposed to low levels of aluminum-fluoride (AlF3) at 0.5 ppm, and
low levels of sodium-fluoride (NaF) at 2.1 ppm ___ approximating
the concentration of 1 ppm elemental fluorine used to fluoridate
Dr. Jensen related that more rats died in the AlF3 group and the
NaF group than the control group; that the aluminum levels in
samples of brain and kidney were higher in both the AlF3 and NaF
groups relative to controls (double the amount of aluminum in the
brain at the lower dose of AlF3 (0.5 ppm) than the higher dose of
AlF3 (50 ppm); and that alterations in the cerebrovasculature, the
frequency of abnormal appearing neurons as well as a reduction in
neuronal density, were greater in animals in the AlF3 group than the
NaF group, and greater in the NaF group than the controls.
Dr. Jensen accentuated that, in haste to determine the neurological
effects, others may have overlooked the existent damage to the
kidney in the AlF3 group and the NaF group compared to controls,
and also the possibility of kidney damage contribution to the neurological
David C. Kennedy, DDS, Past President, International Academy of
Oral Medicine and Toxicology, presented a common sense approach
to reviewing the evidence of fluoride's effect on dental health,
and the scientific literature linking fluoride to higher incidence
of hip fracture.
Dr. Kennedy illustrated that when accounting appropriately for
duration of exposure, and the importance of considering the
highly-susceptible bone remodeling activity of women during
menopause, and the relatively low bone remodeling activity after
menopause, the scientific literature confirms fluoride's positive
correlation to hip fracture.
Dr. Kennedy described the distortion in the classifications
of dental fluorosis that allows proponents to claim that no
adverse health effects occur at 1 ppm when in fact the very graphs
that are used to support this statement show 35% of the children
suffer from mischaracterized mild to very mild dental fluorosis, and
thus possibly any corollary adverse effects such as IQ damage.
Dr. Kennedy placed into perspective the extended risk to which an
infant on formula is exposed, compared to an infant who is not
exposed to fluoride in breast milk. Providing an example of an
infant weighing 4 kg (app. 8.8 lbs) that drinks 1 liter of
water-based formula per day containing 1 mg/L of fluoride, the
child is exposed to 0.25 mg/kg per day, which is 6 times the
0.04 mg/kg day that is accepted as a dose at which dental fluorosis
occurs. As a further common-sense perspective Dr. Kennedy explained,
should the child continue to drink this amount, the child will
consume the presumed lethal dose for one day (5 mg/kg) every 20 days.
Dr. Kennedy cited a study of the 1994 and 1995 California Medi-Cal
data that shows that, after 45 years of fluoridation, the
fluoridated counties cost the state of California significantly
more for dental care per eligible recipient than the non fluoridated
counties; supporting the study by Cornelius Steelink that showed an
increase in dental caries, rather than a decrease in dental caries
when fluoride ingestion is increased, and refuting the claim of
significant dental benefit.
J. William Hirzy, Ph.D., Senior Vice President, Chapter 280
National Treasury Employees Union, and Robert J. Carton, Ph.D.,
Past President, represented the union that consists of and represents
all of the scientists and other professionals at US EPA headquarters,
Washington, DC. They presented a review of the history of the
ethical demands placed on EPA employees to write regulations based
on reviews of fluoride toxicity that were blatantly false; the Agency's
subsequent use of outside contractor scientists, who ignored adverse
data on fluoride to write fluoride regulation support documents;
the EPA's refusal to resolve the issue, and the court's denial of
the union's motion to join as a friend of the court (Amicus Curiae)
in a lawsuit against EPA's fluoride regulations; and the union's
response to public requests for accurate scientific bases for the
Dr. Hirzy presented a comprehensive review of the risk assessment
process, addressing scientific evidence of fluoride's absorption,
acute effects, reproductive toxicity, mutagenic effects,
neurotoxicity, increased hip fracture rate, decreased bone integrity,
skeletal fluorosis, dental fluorosis, osteosarcoma, and claims of
fluoride as an essential nutrient.
Dr. Hirzy displayed three reference dose calculations for
fluoride based on different peer-reviewed toxicity studies.
The first, 0.00015 mg/kg-day, was based on findings of Eckerlin et al.
and Maylin et al. on increased abortion rates and calf death in
cattle. The second, 0.000007 mg/kg-day, was based on findings of
changes in brain morphology and increased IgM inclusions in
cerebrovasculature of rats by Varner et al. The third, 0.0001 mg/kg-day,
was based on findings of diminished IQ in children by Zhao et al.
Dr.Hirzy also presented calculations on the potency of sodium
fluoride as a carcinogen with a potency slope factor of 0.1
Dr. Hirzy and Dr. Carton concurred that a non biased and well-informed
scientific review of the evidence, with the intent of assuring the
safety of the public as required by the oath that EPA scientists take
when assuming their jobs, would establish a Public Health Goal for
Fluoride of 0.0 mg/L (0.0 ppm).
Panel discussions with Q&A totaled an additional 5 hours. Video tapes,
and two-inch binder syllabus may be purchased by calling (800) 728-3833.
The Sponsors of the Symposium:
The Preventive Dental Health Association, a California non-profit
educational corporation; The International Academy of Oral
Medicine and Toxicology; and University of California San Diego,
School of Medicine*.
* After reviewing the program, providing written approval, requiring
that each document and brochure display their sponsorship and
accreditation program, and reviewing the specific brochure prior
to a mailing to 15,000 physicians and dentists, UCSD sent two
contradicting letters denying their approval, and left the continuing
education credits in question.
The California Board of Dental Examiners, in response to an anonymous
complaint, denied continuing education credits for any dental
personnel or dentists attending this symposium on the grounds that
this course, Drinking Water Fluoridation and Ingested Fluoride--Risk
Assessment "...appears to be in the domain of public health and not
enhancing the licentiates ability in the delivery of dental services."