Confirmation of and explanations for elevated blood lead and other disorders in children exposed to water disinfection and fluoridation chemicals

This paper includes detailed rebuttals to the following papers, which allege “virtually complete dissociation” of silicofluorides into harmless silica and fluoride compounds: Urbansky and Schock, 2000; Macek et al., 2006; Morris/Finney et al., 2006.

Coplan MJ, Patch SC, Masters RD, Bachman MS.  Neurotoxicology. 2007 Sep;28(5):1032-42.


Silicofluorides (SiFs), fluosilicic acid (FSA) and sodium fluosilicate (NaFSA), are used to fluoridate over 90% of US fluoridated municipal water supplies. Living in communities with silicofluoride treated water (SiFW) is associated with two neurotoxic effects:

(1) Prevalence of children with elevated blood lead (PbB > 10 μg/dL) is about double that in non-fluoridated communities (Risk Ratio 2, χ2 p < 0.01). SiFW is associated with serious corrosion of lead-bearing brass plumbing, producing elevated water lead (PbW) at the faucet. New data refute the long-prevailing belief that PbW contributes little to children’s blood lead (PbB), it is likely to contribute 50% or more.

(2) SiFW has been shown to interfere with cholinergic function. Unlike the fully ionized state of fluoride (F-) in water treated with sodium fluoride (NaFW), the SiF anion, [SiF6]2- in SiFW releases F- in a complicated dissociation process. Small amounts of incompletely dissociated [SiF6]2- or low molecular weight (LMW) silicic acid (SA) oligomers may remain in SiFW. A German PhD study found that SiFW is a more powerful inhibitor of acetylcholinesterase (AChE) than NaFW. It is proposed here that SiFW induces protein mis-folding via a mechanism that would affect polypeptides in general, and explain dental fluorosis, a tooth enamel defect that is not merely “cosmetic” but a “canary in the mine” foretelling other adverse, albeit subtle, health and behavioral effects. Efforts to refute evidence of such effects are analyzed and rebutted.

In 1999 and 2000, senior EPA personnel admitted they knew of no health effects studies of SiFs. In 2002 SiFs were nominated for NTP animal testing. In 2006 an NRC Fluoride Study Committee recommended such studies. It is not known at this writing whether any had begun.

Incomplete dissociation of [SiF6]2−

“As measured by ion selective electrode without adding “TISAB”, only 2/3rds of the F− bound in [SiF6]2− was detected. The balance was present either in partially dissociated [SiF6]2− such as [SiF2(OH)4]2− or in some fluorinated SA species.”

“The Ion Selective Electrode (ISE) method to measure ionic F in the water plant involves sample dilution with an equal volume of Total Ionic Strength Adjustment Buffer (TISAB). The 2:1 dilution per se causes some dissociation but TISAB also carries a chelating agent to break up fluoride complexes. Other agents control pH at 5.5. None of this is replicated in water plant treatments and certainly not in the digestive tract. Thus, it is unlikely the free F ion levels read on an ISE meter faithfully reflect SiF dissociation status in water leaving the plant, at the faucet, or in the digestive tract.”

“[Kick et al., 1935] and [Zipkin et al., 1956] results imply that soft tissue of young male mammals suffer more exposure to F− from SiFW than NaFW. This is consistent with reversible equilibrium chemistry since the fluoride-bearing dissociation species in SiFW should undergo re-association at stomach pH around 2, regenerating membrane-permeable fluorinated silicic acid (SA) derivatives that would not be produced from NaFW.”

Consequence of “virtually complete” dissociation

“…an EPA Information Sheet defined “virtually complete” dissociation of [SiF6]2− as 99%. This was based on a study that reported 99% dissociation at 1 ppm but it also reported only 95% dissociation at 2 ppm.

“At 99% dissociation, six of the 600 fluorine atom originally bound in 100 [SiF6]2− anions remain bound to silicon in some species. If these fluorines are distributed randomly over 100 silicons, 6% of the 100 pre-dissociation [SiF6]2− anions remain as some fluorine-bearing species. Without stipulating any particular one, it is reasonable to assume that if that species mobilizes a lead atom it does so 1 to1. The atomic weight of lead being about ten times that of fluorine, for each ppm of silicon-bound fluorine, 10 ppm of lead would be mobilized.

“With 1 ppm of free F− and 1% of initial bound F− remaining bound, 10 ppb (ie 0.01 ppm) of F− would be in the lead mobilizing species, so 100 ppb of lead would be mobilized. For reasons discussed in Maas et al., many water systems deliver water with 1.5–2 ppm of F− which should magnify the 100 ppb several-fold. PbW at 100 ppb has been estimated to increase an infant’s PbB by 15 μg/dL and school age children’s by 2.5 μg/dL. A recent mega-study (Lanphear et al., 2005) reports that PbB at 2.5 μg/dL reduces a child’s IQ measurably.”

“When a stream of concentrated FSA or NaFSA enters water, [SiF6]2− dissociates, releasing SA and F− in close proximity and F− catalyzes SA “oligomerization”. Hydrogen bonding sites of linear SA oligomer molecules are spaced apart the same distance as polypeptide backbone repeat units. Properly juxtaposed, they are likely to zip together, creating the “mis-folded proteins” described by Ellis (2002) and Temussi et al. (2003). Protein mis-folding would explain SiFW non-competitive enzyme inhibition as well as other health problems associated with blood-borne polypeptides.”

Implications of increased lead in drinking water

“The effect of PbW on elevated PbB in children has been underestimated on several counts: (a) a fetus in utero is exposed to lead in the mother’s blood released from her bones and/or ingested with her food and drink; (b) a newborn ingests more water per pound of body weight than an adult; (c) all children absorb more of the lead they ingest than adults; (d) their developmental state renders them more susceptible to neurotoxic damage; (e) lead in drinking water extracted from brass plumbing fixtures by combinations of disinfection and fluoridation chemicals is more important than previously thought and has not had the attention it deserves.”

“A fetus will get lead from placental blood due to PbW in a mother’s current diet or released from her bones absorbed many years earlier. The worst and most likely irreversible lead damage is done to a fetus in the first trimester.”

“A breast-fed infant may ingest lead in its mother’s milk; a formula-fed infant’s diet may include tap-water lead, and any child may ingest PbW in home- or commercially-prepared foods. PbW contributes at least half of an infant’s PbB. PbW should be considered as important as lead paint and low calcium intake as a factor in PbB, particularly for Blacks.”

Kidney damage

“Both acute short-term high level F− and chronic low level F− exposures impair calcium-dependent processes, including those associated with neural as well as kidney functions. This is consistent with the damage found in squirrel monkeys exposed to SiFW at 1–5 ppm F− for 18 months. Early development of rat kidney is very sensitive to toxic insult with hypertension later in life a probable outcome of damage inflicted in utero. The same F− levels impairing rat kidney phospholipid cell membranes is associated with dental fluorosis.”


“The role of silicofluorides with significant capacity for enzyme inhibition and other bio-activity adverse to neural health, among other problems, has not been properly explored. On the other hand, several studies designed to rebut this conclusion not only fail to do so, they provide evidence of its validity.”