Silicofluorides Should Not Be Added to Municipal Water Without Safety Testing Adequate to Protect Children and Other Vulnerable Populations

by Myron Coplan, P.E., & Robert Carton, Ph.D.

Resolution submitted to the American Public Health Association, October 21-25, 2001.

The American Public Health Association,

Recognizing that the APHA has had a consistent and long-standing policy of endorsing water fluoridation as a public health measure in Policy Statements 5005, 5508, 5607, 5904, 6912, 8402, and 7911, and

Recognizing also that said endorsement has traditionally been predicated on the belief that fluoride is a valuable caries preventive whose benefits can be enjoyed without adverse health effects by regular ingestion of water treated to an appropriate level of fluoride ion derived from an appropriate source, and

Recognizing that none of the recited APHA Policy Statements took into account the fact that there had been no health safety testing of specific water fluoridating agents known as the silicofluorides (H2SiF6 and Na2SiF6, henceforth “SiFs”) when their use began; and

Recognizing that water systems providing 91 percent of U.S. fluoridated water, and serving 140 million people, 1 dispense 200,000 tons per year of SiFs 2 and these agents have been used since 1947 3 without tests of their health safety 4, 5 and

Recognizing that a 1952 request by a Select Congressional Committee (82nd Cong., 2d Session) for studies “to determine the long-range effects upon the aged and chronically ill of the ingestion of water containing inorganic fluorides” 6 has yet to be addressed regarding health safety of the silicofluorides while animal health studies of fluoridated water, including those conducted by the National Institute of Health's National Toxicology Program, regularly employ sodium fluoride (NaF), the first fluoridating compound used (in 1945), and not SiFs, the principal agents currently added to water; 7,8,9,10,11,12,13,14,15,16 ; and

Further recognizing that, claims to the contrary,17 SiF treated water is not like NaF treated water because [SiF6] 2- (a) is unlikely to dissociate completely under water plant conditions, producing only free fluoride and silicic acid without side reactions;18, 19 (b) is likely to react with Al(OH)3 to produce several derivative compounds; (c) dissociation status depends on pH and concentration so that incompletely dissociated SiF residues may re-associate both at intra-gastric pH around 2.0 20 and during food preparation, producing SiF species including silicon tetrafluoride, (SiF4), a known toxin; 21, 22, 23, 24, 25, 26 and (d) commercial SiFs are likely to be contaminated with fluosiloxanes, 27 arsenic and heavy metals, 28 and radionuclides,29 since they are waste products from fertilizer manufacture and uranium extraction from phosphate rock 30, 31, 32, 33

Recognizing that in 1950,34 the U.S. Public Health Service endorsed Na2SiF6 as a cheaper alternative for NaF, reasoning that equal fluoride uptake by hard tissues demonstrated the biological equivalence of NaF and Na2SiF6, although earlier animal studies 35 had shown that when equal amounts of fluoride were ingested and the total amount of fluoride excreted was also equal, animals exposed to NaF eliminated more fluoride in feces, while animals exposed to Na2SiF6 eliminated three-fold more fluoride in urine, thus indicating circulating blood fluoride levels; and

Recognizing that a 1975 German study found that acetylcholinesterase inhibition, (the intended action of the high-risk organophosphate and carbamate pesticides widely used in agriculture and around residences), is many-fold more severe due to the SiF complex (and other complexes such as with iron) as compared to the simple fluoride ion released by NaF, which is itself an acetylcholinesterase inhibitor;36 and

Noting that dental fluorosis (pre-eruption F-induced tooth enamel malformation) expected in 1945 to be only mild and prevail at 10-12 percent in “optimally” fluoridated areas,37 now averages over 25 percent, and sometimes exceeds 80 percent in said “optimally” fluoridated areas with many moderate to severe cases;38 and

Further noting that a 1983 expert panel appointed by the Surgeon General to review “non-dental health effects” of ingested fluoride was instructed to limit its scope to “death (poisoning), gastrointestinal hemorrhage, gastrointestinal irritation, arthralgias, and crippling fluorosis” thus essentially ignoring many possible effects in children; 39 and

Considering that data on 400,000 children in New York, Massachusetts, and in the NHANES III (National Health and Nutrition Examination Survey III) study, found that where local water is fluoridated with SiFs the prevalence of children with venous blood lead exceeding 10mcg/dL was significantly higher than in non-fluoridated areas with risk ratios of between 2.0 and 4.0 (p<0.001) controlling for race, housing age, poverty, congestion, and parental education);40, 41and

Recognizing that blood lead is believed responsible for adverse effects inflicted in utero such as impaired immune capacity,42 brain damage and developmental problems,43, 44, 45 as well as in early childhood,46, 47, 48, 49, 50, 51and into puberty/adolescence as impaired cognition and impulse control,52, 53and adulthood as nephropathy and hypertension,54, 55and into geriatric life;56 and

Finally, recognizing that dental caries prevalence rates in “optimally fluoridated” areas today is indistinguishable from prevalence rates in non-fluoridated areas 57, 58, 59, 60, 61, 62, 63; and

Noting that the Journal of the American Dental Association has recently published a comprehensive study showing that ingestion of fluoride does not benefit teeth in their pre-eruptive stage, but only via by topical contact after tooth eruption;64 and

Noting also that seven times in the past APHA has in one way or another endorsed fluoridation of public water supplies but none of the relevant POLICY STATEMENTS explicitly endorsed any specific fluoridating agent, whereas POLICY STATEMENT 6912 implicitly did so by identifying fluoridation in Grand Rapids in 1945 which, according to Reference 3, was initially accomplished by adding sodium fluoride to its water supply; and

Noting, moreover, that less than 10% of US fluoridated water today is treated with sodium fluoride while over 90% is treated with one of the SiFs which have never been tested for health safety; and

Further noting that the premise that “fluoride is fluoride” whatever its source is false and dangerously misleading based on evidence that water treated with SiFs is not just like water treated with sodium fluoride as confirmed by (a) epidemiological analyses of several health and behavioral effects comparing communities using SiFs with communities using sodium fluoride or not adding fluoride; (b) biological studies comparing effects of ingested water treated with sodium fluoride with effects of ingested water treated with SiFs; (c) disputed assurances concerning the “virtually total” dissociation of the SiFs under real use conditions; (d) an advisory letter from the Director of the EPA Water Supply and Water Resources Division in a letter67 dated March 15, 2001 summarizing the position of the highest scientific authorities of the EPA reached in January 2001 which notes the following:

“Several fluoride chemistry related research needs were identified including; (1) accurate and precise values for the stability constants of mixed fluorohydroxo complexes [read “silicofluoride dissociation residues”] with aluminum (III), iron (III) and other metal cations likely to be found under drinking water conditions and (2) a kinetic model for the dissociation and hydrolysis of fluosilicates and stepwise equilibrium constants for the partial hydrolysis products.”

thus admitting that EPA scientific leaders are not satisfied with assurances given by their own technical staffs of the health safety of SiFs on two counts: (i) possible formation of toxic complexes with aluminum, iron and other cations commonly present in water plant water and (ii) potential toxic effects from SiF dissociation residues in municipal drinking water that may be present despite predictions made by EPA and others for SiF dissociation.

Citing APHA's explicit endorsement of the precautionary principle as a cornerstone of preventive public health policy, especially in “order to protect the health and well-being of all developing children”;65 and Presidential Executive Order #13045 calling on all federal agencies to ensure that all federal environmental health policies and regulations consider the special sensitivities and vulnerabilities of children;66

The APHA, therefore:

  1. Calls for the establishment of an APHA study committee comprising an equal number of members from the Environment and Oral Health Sections plus a representative of the APHA Directorship to investigate in depth water fluoridation using silicofluorides on the basis that they have never been tested for health safety in humans and may be particularly hazardous to children, the aged and the chronically ill;
  2. Calls for the National Institute of Environmental Health Science/National Toxicology Program to nominate the silicofluorides for priority CCL status to undertake a full battery of chronic health effects testing of silicofluoride treated water; and
  3. Calls for the US. EPA to review its standards for the safe level of fluoride exposure in the light of any NTP results arising under actions requested above.


Myron J. Coplan, P.E.* (APHA #9774108)
Intellequity Technology Services
Natick, MA 01760
(ph) 508-653-6147 (fax) 508-655-3677

Robert J. Carton, Ph.D.** (APHA #9774839)
Environmental Coordinator
U.S. Army Medical Research & Materiel Command
Fort Detrick, MD 21702-5012
(ph) 310-610-2004 (fax) 1-301-619-7803

* Contact author

**The views presented in this resolution are those of its authors (MJC and RJC) and do not necessarily represent the views of the Department of Defense.



(1) United States Department of Health and Human Services; Centers for Disease Control (CDC) Fluoridation Census, 1992, Sept 1993.

(2) Reeves TG; "Water Fluoridation; A Manual for Water Plant Operators"; US Public Health Service, CDC Division of Oral Health, April 1994.

(3) Council on Dental Health , American Dental Association; "Fluoridation in the Prevention of Dental Caries"; Third Edition, 1953.

(4) Letter to the Honorable Ken Calvert, Chairman of the Subcommittee on Energy and the Environment of the House Committee on Science, from EPA Assistant Administrator J. Charles Fox, June 23, 1999.

(5) Personal letter to Dartmouth Professor Roger D. Masters, from Robert C. Thurnau Chief, EPA Treatment Technology Evaluation Branch, November 16, 2000.

(6) Wollan M; "Controlling The Potential Hazards of Government-Sponsored Technology": The George Washington Law Review; V 36 No. 5; pages 1105-1119, July 1969.

(7) Bucher JR, et al; "Results and conclusions of the National Toxicology Program's rodent carcinogenicity studies with sodium fluoride" Int J Cancer; 48(5):733-7, July 9,1991.

(8) Heindel JJ, et al; “Developmental toxicity evaluation of sodium fluoride administered to rats and rabbits in drinking water”; Fundam Appl Toxicol;30(2):162-77, Apr. 1996.

(9) Sprando RL, et al; "Testing the potential of sodium fluoride to affect spermatogenesis: a morphometric study"; Food Chem Toxicol.; 36(12):1117-24, 1998.

(10) Sprando RL, et al; "Testing the potential of sodium fluoride to affect spermatogenesis in the rat"; Food Chem Toxicol.;35(9):881-90, 1997.

(11) Collins TF, et al; "Developmental toxicity of sodium fluoride in rats"; Food Chem Toxicol. ;33(11): 951-60, 1995.

(12) Dunipace AJ et al: "Chronic fluoride exposure does not cause detrimental, extraskeletal effects in nutritionally deficient rats"; J Nutr; 128(8):1392-400, 1998.

(13) Dunipace AJ et al; "Effect of chronic fluoride exposure in uremic rats"; Nephron; 78(1):96-1031, 1998.

(14) Dunipace AJ et al, "Effect of aging on animal response to chronic fluoride exposure"; J. Dent Res;74 (1) 358-368, 1995.

(15) Li YM, et al; "Genotoxic evaluation of chronic fluoride exposure: sister-chromatid exchange study"; J Dent Res;68(11):1525-8, 1989.

(16) Jackson RD et al; "Lack of effect of long-term fluoride ingestion on blood chemistry and frequency of sister chromatid exchange in human lymphocytes"; Environ Mol Mutagen;29(3):265-71, 1997.

(17) Feldman I, Morken D and Hodge HC; "The State of Fluoride in Drinking Water"; J. Dent Res. Vol 36 (2); 192-202,; 1957.

(18) Crosby NT; "Equilibria of Fluosilicate Solutions with Special Reference to The Fluoridation of Public Water Supplies"; J Appl Chem; v19; pp 100-102, 1969.

(19) Busey RH et al; "Fluosilicate Equilibria in Sodium Chloride Solutions from 0 to 60 o C"; Inorg. Chem V 19; pp 758-761, 1980.

(20) Ciavatta L, et al; “Fluorosilicate Equilibria in Acid Solution”; Polyhedron Vol 7 (18);1773-79;1988

(21) Gabovich RD; "Fluorine in Stomatology and Hygiene"; translated from the original Russian and published in Kazan (USSR); printed by the US Govt Printing Office on behalf of the Dept of Health Education and Welfare. US Public Health Service, National Institute of Dental Health; DHEW pub no (NIH) 78-785, 1977.

(22) Roholm K; "Fluorine Intoxication; A Clinical-Hygiene Study"; H. K. Lewis & Co. Ltd, London; 1937.

(23) Lewis RJ, jr.; "Hazardous Chemicals Desk Reference": Van Nostrand Reinhold; Fourth Edition.

(24) Matheson Gas Products; 30 Seaview Drive, Secaucus, NJ; "Effects of Exposure to Toxic Gases" and MSDS for CAS # 7783-61-1; created 1/24/89.

(25) Voltaix, Inc.; Material Safety Data Sheet for Silicon Tetrafluoride (SiF4).

(26) Rumyantseva GI et al; "Experimental Investigation of The Toxic Properties of Silicon Tetrafluoride"; Gig Sanit ;(5):31-33, 1991.

(27) Ricks GM et al; "The Possible Formation of Hydrogen Fluoride from the Reaction of Silicon Tetrafluoride with Humid Air": Am. Ind. Hyg. Assoc. J. (54); 272-276, 1993.

(28) Craig JM; "Fluoride Removal from Wet-Process Phosphoric Acid Reactor Gases"; Ph. D. Dissertation; Univ. Fla. at Gainseville, 1970.

(29) Murray RL; “Understanding Radioactive Waste”; Third Ed.(ed Powell JD); 1982

(30) Becker Pierre; "Phosphates and Phosphoric Acid: Raw materials, technology, and economics of the wet process"; Marcel Dekker: New York (First ed.) 1983, Second ed., 1988.

(31) Slack AV; "Phosphoric Acid"; Part I; Marcel Dekker: New York, 1968.

(32) Greek BF, Allen OW, and Tynan DE; "Uranium Recovery from Wet Process Phosphoric Acid"; Industrial & Engineering Chemistry; vol 49 (4); 628-636, 669-671, 1957.

(33) Rahn FJ et al; “A Guide to Nuclear Power Technology”; John Wiley & Sons' New York; 1984

(34) McClure FJ: "Availability of Fluorine in Sodium Fluoride vs, Sodium Fluosilicate"; Public Health Reports vol 65 No 37; 1175-86; 1950.

(35) Kick CH et al; "Fluorine in Animal Nutrition"; Bulletin 558, Ohio State Agricultural Experiment Station, Wooster OH, November 1935.

(36) Westendorf J; "Die Kinetik der Acetylcholinesterasehemmung und Die Beeinflussung der Permeabilitat von Erythrozytenmembranen durch Fluorid und Flurocomplex-Jonen"; Doctoral Dissertation, Universitat Hamburg Fachbereich Chemie; Hamburg; 1975

(37) Dean HT; "Endemic Fluorosis and its Relation to Dental Caries"; Public Health Report 53; 1443-52; 1938.

(38) National Research Council; "Health Effects of Ingested Fluoride"; Subcommittee on Toxicology, Board on Environmental Studies and Toxicology, Commission on Life Sciences, National Academy Press: Washington, DC, 1993.

(39) Koop CE, Letter to William D. Ruckelshaus, Administrator, EPA, dated Jan 23, 1984 and transcript of Proceedings of Surgeon General's Ad Hoc Committee on "Non-Dental Health Effects of Fluoride"; April 18-18, 1993, Jay R. Shapiro, Chairman.

(40) Masters RD and Coplan MJ; “Water Treatment with Silicofluorides and Lead Toxicity”; Int. J. of Environ. Studies; 56; 435-449, 1999.

(41) Masters RD, Coplan MJ, Hone BT, and Dykes; "Association of Silicofluoride Treated Water with Elevated Blood Lead"; NeuroToxicology 21 (6), 2000.

(42) Miller TE et al; “Developmental Exposure to Lead Causes Persistent Immunotoxicity in Fischer 344 Rats”; Toxico Sci. 42; 129-135; 1998.

(43) Chanez C, et al; “Effect of lead on Na+,K+ATPase activity in the developing brain of intra-uterine growth-retarded rats”; Neurochem Pathol; 5(1):37-49; 1986.

(43) Dietrich KM et al; “Low-Level Fetal Lead Exposure Effect on Neurobehavioral Development in Early Infancy”; Pediatrics; Vol 89 no. 5, 1987.

(44) Aschengrau A et al; “Quality of Community Drinking Water and The Occurrence of Late Adverse Pregnancy Outcomes”; Arch Environ Health ; vol 48 no. 2; 105-13, Mar-Apr 1993.

(45) Needleman HL; “Low-Level Lead Exposure and the IQ of Children”; JAMA ; Vol 263 no. 5; Feb 2, 1990.

(46) McMichael AJ et al; “Port Pirie Cohort Study: Environmental Exposure to Lead and Children's Abilities at the Age of Four Years”; New Eng J of Med ; vol 319 no. 8; Aug 25, 1988.

(47) Kim R, et al; “A longitudinal study of chronic lead exposure and physical growth in Boston children”; Environ Health Perspect ; 103(10):952-7, 1995.

(48) Leviton A, et al; “Pre- and postnatal low-level lead exposure and children's dysfunction in school”; Environ Res ; 60(1); 30-43, 1993.

(49) Schoen EJ; “Neuroendocrine effects of toxic and low blood lead levels in children”; Pediatrics ; vol 92 (3), 1993.

(50) Eppright TD, et al; “Attention deficit hyperactivity disorder, infantile autism, and elevated blood-lead: a possible relationship”; Mo Med ; 93(3); 136-8, 1996.

(51) Walker SW III; “The Hyperactivity Hoax”; St. Martin's Press; New York, Dec 1998.

(52) Bellinger DC, et al; “Low-level lead exposure, intelligence and academic achievement: a long-term follow-up study”; Pediatrics ; vol. 90 (6); 885-61,1992.

(53) Loghman-Adham M; “Renal effects of environmental and occupational lead exposure”; Environ Health Perspect ; 105(9); 28-39; 1997.

(54) Korrick SA, et al; “Lead and hypertension in a sample of middle-aged women”; Am J Public Health; 89(3); 330-5, 1999.

(55) Vig EK, and Hu H; “Lead toxicity in older adults”; J Am Geriatr Soc ;11):1501-6, 2000.

(56) Watson GE, et al; “Influence of maternal lead ingestion on caries in rat pups”; Nat Med;3(9): 1024-5, 1997.

(57) Brunelle, JA and Carlos JP; "Recent Trends in Dental Caries in US Children and Effect of Water Fluoridation"; J. Dent. Res 69 Spec Iss; 723-27, 1990.

(58) Kobayashi S et al; "Caries Experience in subjects 18-22 years of age after 13 years' discontinued water fluoridation in Okinawa"; Community Dent Oral Epidemiol; 20(2):81-3; 1992.

(59) Kumar JV et al; "Changes in Dental Fluorosis and Dental Caries in Newburgh and Kingston, New York"; Am. J. Pub. Hlth. Vol 88, No 12; 1866-70, Dec 1998.

(60) Kumar JV and Greene EL; "Recommendations of Fluoride Use in Children"; NYSQJ, Feb 1998.

(61) Kunzel W and Fischer T; “Caries prevalence after cessation of water fluoridation in La Salud, Cuba”; Caries Res; 34(1):20-5; 2000 Jan-Feb.

(62) Burt BA, Keels MA, Heller KE; “The effects of a break in water fluoridation on the development of dental caries and fluorosis”; J Dent Res.;79(2):761-9, 2000.

(63) Seppa L, Karkkainen S, Hausen H; “Caries in the primary dentition, after discontinuation of water fluoridation, among children receiving comprehensive dental care”; Community Dent Oral Epidemiol;28(4):281-8, 2000.

(64) Featherstone JDB; "The Science and Practice of Caries Prevention"; JADA Vol 131

(65) The Precautionary Principle and Children's Health, Policy Statement #200011 Adopted by the Governing Council of the American Public Health Association, November 15, 2000.

(66) Presidential Executive Order #13045, Protection of Children from Environmental Health Risks and Safety Risks, Signed April 21, 1997.

(67) Letter dated March 15, 2001 from Sally C. Gutierrez, Director, Water Supply and Water Resources Division, US EPA National Risk Management Laboratory, to Roger D. Masters, Dartmouth College.