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Scientific Risk Assessment Of Drinking Water Fluoridation and Health Effects
of Ingested Fluoride
A Summary 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 adequate margin-for-safety.
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 policy.
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 conclusion.
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 benefit.
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 fluorine-containing pesticides.
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.
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.
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 development.
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. Dr. Krook
explained that 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 poisoning.
Karl Jensen, Ph.D., Neurotoxicological Division, National Health and
Environmental Effects Research Laboratory, US EPA, Triangle Research 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 drinking water.
Dr. Jensen related that more rats died in the AlF3group 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 effects.
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.
Robert J. Carton, Ph.D.
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
union's position.
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 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 (mg/kg-day)-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).
| The
Sponsors of this Symposium |
The Sponsors of this 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
actions, 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."
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