A Review of the Ingested Fluoride
Scientific Risk Assessment Symposium

by Mark D. Gold

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:

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. 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, 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 drinking water.

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 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., 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 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 (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).

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."