Fluoride Action Network

Sulfuryl Fluoride – FAN’s first Objection & Request for Hearing, April 8, 2002

Fluoride Action Network | April 8, 2002

Written Objections and Request for Hearing in the matter of:

Sulfuryl fluoride; Temporary Pesticide Tolerances. Final Rule.

Docket control number OPP-301166A

Submitted by

Ellen and Paul Connett
82 Judson Street, Canton New York 13617
Tel: 315-379-9200. Fax: 315-379-0448
Email: wastenot@northnet.org

April 8, 2002

Note: Some of the online links cited in the original submission are no longer active.
We have updated them as of August 2003


We wish to appeal the US EPA’s granting of a Temporary Pesticide Tolerance to Dow for residue limits of fluoride on raisins and walnuts from the use of sulfuryl fluoride as a fumigant. Our appeal is based upon the following:

1. Fluoride is persistent, toxic, and bioaccumulates in humans. It also bioaccumulates in farm animals, wildlife, and soil. Bioaccumulation is one of the important intrinsic properties of a chemical substance. Long-term exposures to fluoride increases the risk to humans and other wildlife for body burdens which will result in adverse health effects. Bioaccumulation is an important concept and should be treated with care. Unfortunately, the EPA has not done this. In fact, EPA does not even mention fluoride’s intrinsic ability to bioaccumulate in humans in its September 5, 2001, health risk assessment on fluoride (1), nor in the Final Rule issued on February 7, 2002. (2)

2. The US EPA is out of date in its review of the literature (as are the agencies it cites) on the toxic effects of fluoride. It needs to look at all the end points of concern based upon a more up-to-date and a more informed review of the literature

2. Even if the US EPA considered only the end point of damage to teeth and bones, current exposure to fluoride is far too high for children and adults. Adults are already close to the Maximum Contaminant Level Goal (0.114 mg/kg/day) and some children are already exceeding it. No new sources of fluoride should be introduced.

3. The US EPA needs to recalculate an up-to-date estimate of the daily dose of fluoride for infants, children and adults.

4. It needs to add the estimated increment from exposure to raisins and walnuts, at the proposed tolerance limits, for a high end user, to these background exposure doses to infants and adults.

5. Until, it has done this rudimentary analysis it is premature for the US EPA to declare that these tolerance limits from the use of sulfuryl fluoride as a fumigant on raisins and walnuts, poses no significant health risk.

6. It is no argument that this is only a temporary permit which will last three years. Within a few days of this ruling DOW came back with a petition (February 15, 2002: Docket control number PF-1068) to establish permanent tolerances for the use of sulfuryl fluoirde on 40 food commodities, most of which were not included in previous cryolite tolerance rulings and with far higher residue tolerances (3). Thus this ruling is setting a very dangerous precedent. It could set in motion a huge new source of fluoride exposure for the American population, at a time when more and more researchers believe that we, and our children, are being overexposed to fluoride. We do not need a new source. Instead we should be looking for ways of reducing our exposure. The US EPA should be encouraging Dow and other chemical companies to find fumigants which neither contribute to ozone layer damage nor add a persistent pollutant to our bodies and the environment.


In terms of the relief sought, the submitters ask EPA to rescind the temporary tolerances granted for sulfuryl fluoride on raisins and walnuts.


Under 40 C.F.R. ¤ 180.33 (m) The Administrator may waive or refund part or all of any fee imposed by this section if the Administrator determines in his or her sole discretion that such a waiver or refund will promote the public interest or that payment of the fee would work an unreasonable hardship on the person on whom the fee is imposed. A request for waiver or refund of a fee shall be submitted in writing to the Environmental Protection Agency, Office of Pesticide Programs, Registration Division (7505C), Washington, DC 20460. A fee of $1,700 shall accompany every request for a waiver or refund, except that the fee under this sentence shall not be imposed on any person who has no financial interest in any action requested by such person under paragraphs (a) through (k) of this section. The fee for requesting a waiver or refund shall be refunded if the request is granted.

1. Outdated Review of the Literature.

According to the US EPA’s ruling:

“there is a reasonable certainty that no harm will result to the general population, and to infants and children from aggregate exposure to sulfuryl fluoride and inorganic fluoride residues.”

This conclusion is based upon outdated data. The EPA is largely basing its conclusions on the 1990 NTP cancer study on rats (4) and is ignoring more recent studies of fluoride’s impact on the pineal gland (Luke, 5, 6); on the central nervous system – Mullenix (7); Gao (8); Zhao (9); Lu (10); on bone fractures, Li et al. (11) and Alarcon-Herrera (12); its interactions, in the presence of the aluminum ion, on G-proteins and hence the signaling mechanism of several water soluble hormones, neurotransmitters and growth factors, Strunecka and Patocka (13). It has further underestimated the significance of the Varner (14) study on rats, as well as ignoring earlier important studies on the thyroid gland – Galletti and Joyet (15) and Bachinskii (16).

With respect to the EPA’s failure to cite studies on the pineal gland, we were surprised that EPA failed to comment on, or acknowledge, that we had sent them Dr. Jennifer Luke’s Ph.D thesis (5) on this very subject. (Ellen Connett sent a copy of the thesis to Dennis McNeilly in November -possibly October- 2001).

The second half of Luke’s thesis (5) examined the effect of fluoride on the production of melatonin in Mongolian gerbils. She showed that the levels of a melatonin metabolite excreted in the urine was significantly lowered in high fluoride treated animals, and the animals showed signs of reaching puberty earlier than controls.

Luke also noted a finding in the health study in the Newburgh-Kingston fluoridation trial (which was not thought significant at the time) that on average the girls in Newburgh started menstruating 5 months earlier than the girls in the control, non-fluoridated, city of Kingston (16-A). Thus one of the risks we may be taking by exposing our whole population to fluoride is interfering with delicate regulatory timing processes, from the onset of puberty to the aging process.

The US EPA cites the following agencies to support their claim that the only two target organs of interest are the bone and the teeth:

“There have been numerous independent evaluations of the toxicity of fluoride: U.S. Public Health Service (1991), EPA (1985), National Academy of Science (NAS) (1998) and Agency for Toxic Substances and Disease Registry (ASTDR) (1993, draft report 2001). All of these reviews have indicated that the critical adverse effects, i.e., the endpoints to regulate, from fluoride ingestion are the effects on bone and teeth.”

We would argue that all of the above reviews are outdated with respect to other health issues, including the draft report 2001 of the ATSDR, which we have critiqued in detail (17). All these reviews have somehow overlooked the key studies on the pineal gland, thyroid gland, the central nervous system, bone fracture and G-proteins we have listed above.

The EPA’s claim that

“It is noteworthy… that the Centers for Disease Control and Prevention lists fluoridation of the drinking water as one of the ten great public health achievements in the 20th Century”

is not noteworthy at all. It was highly predictable. While we do not want to enter into the fluoridation “debate” with our objection to the Final Rule for Sulfuryl fluoride use on raisins and walnuts, we offer the following brief comments. The CDC’s claims (18, 19) of the huge benefits to teeth from water fluoridation ignore the fact that most European countries do not fluoridate their public drinking water systems and yet according to data from the World Health Organization (WHO, 20) the teeth of European children are just as good, if not better than the teeth of American children. More importantly in both the 1999 and 2001 reports (18, 19) the literature cited by the CDC to dismiss health concerns is six years out of date. The public has the right to expect that agencies, which are working on their behalf to protect their health, be on top of the literature, not lagging far behind. We enclose a critique by Connett and Connett (21) of the CDC report published in 2000.

EPA states:

“In addition, fluoridation of water has been endorsed by the U.S. Surgeon General”

When the US Public Health Service first endorsed water fluoridation in 1950 before one single trial had been completed (not a scientifically defendable act), they did so using the US Surgeon General. Every successive US Surgeon General has been trotted out on a regular basis to continue to promote this policy. It is a bit like Michael Jordan endorsing Nike shoes. The US Surgeon General’s opinions on this matter have no more substance than the reports on which they are based. These reports have to be judged on the basis of the quality of the science mustered in the defense of the arguments produced. This is essential if we are to keep as the key determinant to government decisions related to public health matters.


When the EPA claims that,

“The exposure to fluoride as a result of the proposed tolerances in or on walnuts and raisins is insignificant compared to the exposure to fluoride in drinking water”

They are making the cardinal mistake of ignoring how close the average American is already to the Maximum Contaminant Limit Goal (MCLG) discussed below. Under these circumstances it is irresponsible to conduct its analysis by comparing the incremental dose (estimated from from raisins and walnut consumption) to some other dose. It is the total dose, which is of concern here. What they should be doing is adding the incremental dose to the range of background doses to fluoride, from all sources, including fluoridated water, to see how close the average individual and the high range individual is getting to the MCLG.

Later in their response the EPA cites some numbers which are helpful in this respect, when they state

“In consideration of the proposed temporary tolerances for walnuts and raisins, the Agency used the maximum concentration limit goal (MCLG) of 4.0 ppm (0.114 mg/kg/day) for fluoride as the basis for a maximum allowable exposure to inorganic fluoride (see the Cryolite Reregistration Eligibility Decision, 8/96, EPA-738-R-96-016). This exposure was used as the chronic population adjusted dose for inorganic fluoride in the risk assessment supporting the temporary tolerances.”

This is a good starting point for what the US EPA should have done in a proper scientifically based analysis designed to be protective of health. The maximum concentration limit (MCLG) that they cite of 0.114 mg/kg/day translates to 8 mg per day for a 70 kg adult. The question then becomes what range of exposure does someone have to fluoride living in a fluoridated community (and most Americans do). One of the agencies that they cite, DHHS (22), actually did this calculation and reported the range to be 1.6 — 6.6 mg per day (Table 11). This means that people in the upper part of that range are already very close to the MCLG of 8 mg per day. A conservative assessment would have added the incremental dose predicted from a high use consumer of raisins and walnuts to the high end of this range and reported how close — how very close- this is to the MCLG.

The situation is even worse for children. The same DHHS study cited above (22) gives the range of exposure for children living in optimally fluoridated communities as 0.9 to 3.6 mg per day (Table 10). Taking the weight of the child in question as 20 kg, would yield dosages ranging from 0.045 to 0.18 mg/kg/day. This puts the child at the high end of this range ABOVE the MCLG of 0.114 mg/kg/day, BY NEARLY 60%. Clearly, children in the US are getting too much fluoride already, they don’t need any more.


The over exposure of our children to fluoride is also disturbingly confirmed by the dental fluorosis rates. In a study by Heller et al (23), based upon data collected in 1986-87 by the NIDR it was found that nearly 1 in 3 (29.9 %) of children living in optimally fluoridated areas had dental fluorosis on at least two teeth. The original goal of the fluoridation program was to hold dental fluorosis to 10% of the population, in its mildest form. A more recent estimate by a team of York University in the UK (24) based upon worldwide figures would put the level of dental fluorosis at 48% of the children in optimally fluoridated communities, with 12.5% at a significant level of seriousness. Again, our children are getting overdosed on fluoride. They do not need any more.

To add another level of seriousness to this analysis, a study conducted by Alarcon-Herrera (12) in Mexico, found a close linear correlation with the severity of dental fluorosis (a good biomarker for fluoride exposure before the eruption of the permanent teeth) and the incidence of bone fracture.

Fein and Cerklewski (25) reported on the fluoride content of certain children’s foods made with mechanically deboned chicken. They state:

“Brand A pureed infant foods prepared from chicken contained 3.22-8.63 ppm F (mean 5.58 ppm); brand B contained 1.89-4.63 F (mean 2.82 ppm)… A significant correlation of calcium with the higher fluoride content of chicken products suggests that the mechanical deboning process was the source of the extra fluoride… Excessive fluoride intake could therefore occur from regular use of these foods, especially when added to other sources of fluoride intake such as fluoridated water, formulas, and beverages prepared from fluoridated water, and fluoridated toothpaste.”

Lewis and Limeback (25-A) found that children up to 11 years of age in North America are being over-exposed to fluoride. The following Table illustrates this:

Table 16: Recommended and actual fluoride intake estimates

Age Group Recommended F Intake
(microgram/kg bw/day)
 Actual F Intake
(microgram/kg bw/day)
Up to 6 months 3 – 71
14 – 93 (formula fed)0.5 – 2.6 (breast fed)
7 months to 4 years 56 – 81
87 – 160 *45 – 96 **
 5 to 11 years 32 – 45
49 – 79 *26 – 44 **
 12 to 19 years 24 – 33 33 – 45 *17 – 21 **
 20 years and over 32 – 41 47 – 58 *32 – 36 **
( ): Upper value to prevent moderate fluorosis * Estimate of actual intake based on consumption of fluoridated water** Estimate of actual intake based on consumption of non-fluoridated water



At the other end of the age range, a recent study by Li et al (26) found that in six Chinese Villages the incidence of hip fracture in the elderly increased in a dose response manner above 1 ppm. Compared to the rate of hip fracture at 1 ppm, the rate doubled for villages above 1.5 ppm and tripled for villages above 4.5 ppm. This study would put into question the adequacy of the MCLG used by the EPA to protect against bone damage.


We were shocked when we read the EPA’ s dismissal of the significance of the Varner et al’s study (14) based upon a conversation that they had had with one of their employees ( Issue #2).

“The commenters do reference new information not considered as part of the Agency’s risk assessment. In particular, one commenter suggested that the Agency incorporate the results of a study entitled “Chronic Administration of Aluminum-Fluoride or Sodium Fluoride to Rats in Drinking Water: Alterations in Neuronal and Cerebrovascular Integrity”, published in the publication Brain Research in 1998 [14]. One of the co-authors of this study is an Agency employee who has indicated that the experiment discussed was designed to explore a specific hypothesis and that the results are not directly applicable to making conclusions about effects of aluminum or fluoride on public health. In addition, the study co-author has indicated that the results of the study do not support a conclusion that aluminum or fluoride selectively damage the brain or that these compounds cause Alzheimer’s Disease. Therefore, at this time, the results of this study are not considered significant from the standpoint of establishing the tolerances proposed in the Agency’s September 5, 2001, proposed rulemaking.”

What kind of scientific process is this? If there is some kind of cogent analysis here they should put it into writing and have it peer reviewed. They might also explain why these comments were not included in the paper that this employee co-authored. Why should scientists go through the process of getting their papers peer reviewed and published, if they are going to be dismantled in this kind of after the fact fashion?

The Varner et al. study was mentioned in a September 5, 2000, letter from EPA Assistant Admistrator J. Charles Fox to the Honorable Ken Calvert. As this letter was cited by EPA in its approval of a Temporary tolerance for sulfuryl fluoride, perhaps it is of some interest to note what it states:

“In l999, EPA convened a group of experts to carefully consider the results of the Varner et al. (1998) study. A copy of the report of that conference is included. As a result of that conference, EPA has requested that the National Toxicology Program consider the possibility of conducting additional studies of the neurotoxicity of aluminum that include verification of the results observed in the Varner et al. study.”

— Note: the full letter is available online at

We understand that the NTP has agreed to conduct the requested studies. What is of relevance in our petition is that the authors of this study speculated that fluoride facilitated aluminum to cross the blood brain barrier.

With so many people concerned about the huge increase in Alzheimer’s Disease in this country, we believe that the US EPA’s dismissal of the Varner et al. study (14) was cavalier. This study showed that when rats were fed either aluminum fluoride or sodium fluoride at a fluoride level of 1 ppm in their drinking water (the same level of fluoride put into the public drinking water in America) it led to kidney damage, brain damage, a greater uptake of aluminum into the brain, and the occurrence of beta amyloid plagues. Beta amyloid is associated with Alzheimer’s Disease.

In EPA’s September 5, 2001 (1) risk assessment of fluoride they found that the majority of adverse effects from animal studies affected the brain. For example:

1. In a 2-generation reproduction inhalation study in rats, vacuolation of the white matter in the brain was observed in the parental animals

2. In 2-week inhalation studies in rats, dogs and rabbits, different target organs were affected… In rabbits the primary target organ was the brain, in which malacia (necrosis) and vacuolation were observed in the cerebrum.

3. In subchronic (90-day) inhalation studies in rats, dogs, rabbits and mice the brain was the major target organ. Malacia and/or vacuolation were observed in the white matter of the brain in all four species. The portions of the brain most often affected were the caudate-putamen nucleus in the basal ganglia, the white fiber tracts in the internal and external capsules, and the globus pallidus of the cerebrum. (In dogs and rabbits, clinical signs of neurotoxicity [including tremors, tetany, incoordination, convulsions and/or hind limb paralysis] were also observed.)

4. In chronic (1-2 year) inhalation studies in rats, dogs and mice, target organs were the same as in the 90-day studies… Other treatment-related effects in rats included effects in the brain (vacuolation) of the cerebrum and thalamus/hypothalamus.

5. In chronic (1-2 year) inhalation studies in rats, dogs and mice, target organs were the same as in the 90-day studies… In dogs and mice, increased mortalities, malacia and/or vacuolation in the white matter in the brain.

6. In a 2-generation reproduction inhalation study in rats, vacuolation of the white matter in the brain…

7. In two exposures on consecutive days for 6 hours/day at 300 ppm vacuolation of the white matter in the cerebrum of the rat was observed.

From the results of the animal studies in EPA’s risk assessment it is clear that the white matter of the brain is under attack.

According to Christopher Filley, author of The Behavioral Neurology of White Matter (Oxford University Press, 2001):

“…the assumption that the singular phenomena of human behavior predominantly require the activities of the cortical gray matter is one of the most pervasive in all of neuroscience. Whereas there is an impressive body of evidence in support of this belief, it is worth recalling that the cerebral cortex consists of only the outermost 3 millimeters of the brain. Moreover, a wealth of clinical experience suggests that disorders affecting structures below the cortex, many of which are white matter tracts, reliably and significantly alter mental functions. Thus, the notion that mental life is exclusively represented in the cortical gray matter should be considered an oversimplification.

“A wide range of syndromes involving both cognitive decline and emotional dysfunction has been linked with structural involvement of the brain white matter. Clinical observations of patients with white matter disorders generate the essential data to support this claim. Much additional information has been gathered with the help of magnetic resonance imaging (MRI), a powerful neuroimaging technique that has provided unprecedented views of the white matter and permitted correlations with neurobehavioral syndromes. These syndromes may equal or surpass in clinical importance the various deficits in motor and sensory function of white matter lesions well known from classical neurology. Whereas caution is still appropriate in assessing the neurobehavioural importance of white matter changes, it is no longer possible to ignore them. (p 3-4)…

“Early clinical features of cerebral white matter involvement typically include confusion, inattention, memory dysfunction, and personality change… Measures of attention, cognitive speed, memory retrieval, visuopatial skills, and executive function are likely to be most sensitive to subtle white matter dysfunction. In contrast to disorders primarily involving the cortex, higher cerebral functions such as language, praxis, and perception are uncommonly affected; the usual preservation of language is an important point because affected individuals may display normal language and thus appear cognitively intact, when in fact they have significant deficits in other neurobehavioral domains (p 249).”

The majority of Filley’s book examines the `Disorders of White Matter,’ which are wide-ranging and include Multiple Sclerosis, HIV dementia, Lupus, Migraine, Hydrocephalus, to name a few.

Such a finding becomes particularly worrying when it is coupled with the fact that fluoride in the presence of aluminum triggers the same response from G-proteins which is triggered by water soluble hormones, some neurotransmitters and growth factors. The G-proteins are a key component for the transmission of signals, which arrive out the outside of the cell, into changes in the inside of the cell. There are some 800 references to this activation of G-proteins in the literature and a good starting point is the review by Strunecka and Patocka (13). This is another huge important area ignored by the US EPA.

This dismissal certainly puts into question the EPA’s objective articulated in this quote:

“The Agency believes that it is important to remember that the objective of the toxicological testing is to define no observed adverse effect levels and lowest observed adverse effect levels for the chemical being evaluated. The Agency has taken all of these studies into account and believes that the toxicological endpoints chosen by the Agency in its risk assessment are sufficiently protective of human health.” ( Issue #1)


We find the EPA’s response to issue #2 particularly unsatisfactory when they say

“Regarding exposure to fluoride via dental products, the Agency believes that warning labels on these products provide explicit direction on how to significantly limit dietary exposure to fluoride-containing dental products for children.”

We disagree. There are millions of Americans who do not have the literacy skills to understand these warnings. According to Literacy Volunteers of America “Facts on Literacy In America”:

“How literate is the adult population? … Almost all adults in Level 1 can read a little but not well enough to fill out an application, read a food label, or read a simple story to a child… Between 21 and 23 percent of the adult population or approximately 44 million people, according to the National Adult Literacy Survey (NALS), scored in Level 1.” (Ref: http://www.literacyvolunteers.org/about/index.htm ).

We are not aware of any toothpaste sold in the US that has warnings in any language other than English. While we could not find a category for literacy in the US Census, the 1990 US Census ranks Spanish in the highest category: “Ranked by Number Who Speak English Less Than ‘Very Well’.” Approximately 8,305,765 people are identified in this category out of a total of 17,339,172. (Ref: http://www.census.gov/population/socdemo/language/table5.txt )

There are significant populations in the US who are at risk from fluoride exposure simply because they do not have ability to read the “explicit direction” on toothpaste products.”

Additionally, the Food and Drug Administration mandated that warnings be placed on toothpaste in 1997. Up until that time the overwhelming majority of Americans were unaware of the risks posed by the ingestion of fluoride-containing toothpastes, which represent probably over 99 percent of toothpaste sold in the US.

Unfortunately, most Americans rely on the government to protect them from harm from ordinary, everyday products that are sold to any age group in the US. According to a 1993 Canadian report (27):

“Dental products that contain fluoride, such as toothpaste, have been identified as significant sources of inorganic fluoride for children and adolescents (page 42).”

According to a 1999 Canadian report (28):

“A recent paper analyzed reports to the American Association of Poison Control Centres (Shulman et al, 1997) of suspected over-ingestion of fluoride from home-use dental products. Children under the age of 6 years accounted for 80% of the reports. Although the outcomes were not serious, many required medical treatment. Fluoridated toothpastes and mouthrinses can result in levels of ingestion that may be toxic. For example, 50 g of 1,000 ppm of toothpaste could result in toxicity in a child of 10 kg body weight. Consequently, products containing fluoride should be kept out of reach of children to prevent these potentially serious levels of ingestion (page 35).”

Other routes of exposure not accounted for.

In 1977 Rose and Marier (29) cited the following study that indicates the concentration of fluoride ion significantly increases in fluoridated water boiled in Teflon-lined cookware. How many parents warm milk or water for their infants in teflon-coated ware? We are not aware of any study published to dispute this finding:

“A study by Full and Parkins (1975) raises the possibility that Teflon-lined cookware may contribute to the fluoride ingested by humans. Full and Parkins boiled fluoridated (1 ppm) water at a moderate rate until a one-third or one-half reduction in volume was attained, then determined the fluoride content of the residual water by ion specific electrode. In aluminum ware, waterborne fluoride concentration was decreased. In stainless steel and Pyrex ware, fluoride ion concentration increased, but to a lesser degree than expected on the basis of volume reduction. In Teflon-coated ware, the concentration of fluoride ion increased to nearly 3 ppm. This result requires confirmation; but, if it is correct, then the release of fluoride into foods during cooking in plastic-coated wares requires investigation.” – (Note: Rose & Marier’s study is available online at: http://www.fluoridealert.org/NRC-fluoride.htm )

When EPA adds that

“Regarding other exposures, the Agency’s risk assessment includes exposures from the ingestion of fluoridated drinking water and fluoride exposures from the use of other pesticides, specifically cryolite. The Agency discussed these considerations at great length in its proposed rule of September 5, 2001”,

we have to ask whether they in fact confirmed what we have discussed above, namely that some children in optimally fluoridated areas are already being exposed to fluoride above the MCLG? Or did they reject the DHHS (Table 10) data (22)?

In fact the EPA in their Sept 5, 2001 risk assessment said that (1)

“Aggregate exposure to inorganic fluoride from sulfuryl fluoride, cryolite, and [[Page 46422]] water fluoridation is estimated to be 0.087 mg/kg/day for the most highly exposed population subgroup (children 1-6 years of age).”

Thus they have opted for a single figure (a mean?) and avoided putting in a number at the high end of the range. This way they were able to report that they had only reached 75% of the MCLG. However, this is misleading. They didn’t include dental products in this calculation, nor food and beverages prepared in fluoridate water, nor fluoride supplements. Why did the US EPA having cited the DHHS (22) study for other purposes, fail to use their calculations to reach a more conservative assessment of children’s current exposure to fluoride.


Until the EPA has addressed the issues identified above scientifically and comprehensively it is highly premature to give a Dow this permit. We therefore appeal their decision to do so for all the reasons listed above.

We are also appending our comments on Dow’s application for tolerance limits for 50 more foodstuffs it plans to fumigate with sulfuryl fluoride. The arguments contained therein will give further detail on the issues raised above and should be considered part of our appeal.


1. EPA. Federal Register. September 5, 2001. Sulfuryl Fluoride; Proposed Pesticide Temporary Tolerances. [OPP-301166; FRL-6799-6]

2. EPA. Federal Register. February 7, 2002. Fluoride; Temporary Pesticide Tolerances. Final Rule. [OPP-301166A; FRL-6823-4]

3. EPA. Federal Register. February 15, 2002. [PF-1068; FRL-6822-2]

4. NTP. National Toxicology Program [NTP] (1990). Toxicology and Carcinogenesis Studies of Sodium Fluoride in F344/N Rats and B6C3f1 Mice. Technical report Series No. 393. NIH Publ. No 91-2848. National Institute of Environmental Health Sciences, Research Triangle Park, N.C.

5. Luke, J. (1997). The Effect of Fluoride on the Physiology of the Pineal Gland. Ph.D. Thesis. University of Surrey, Guildord, U.K.

6. Luke J (2001). Fluoride deposition in the aged human pineal gland. Caries Res. 35:125-128.

7. Mullenix P et al. (1995). Neurotoxicity of sodium fluoride in rats. Neurotoxicology and Teratology, 17, 169-177.

8. S Li, JL Zhi, Gao RO (1996). Effect of fluoride exposure on intelligence in children. Fluoride 28(4): 189-192.

9. Zhao LB et al (1996). Effect of high-fluoride water supply on children’s intelligence. Fluoride, 29, 190-192.

10. Lu, Y. et al. (2000). Effect of high-fluoride water on intelligence of children. Fluoride, 33, 74-78.

11. Li Y, C.Liang et al. (1999). Effect of long-term exposure to fluoride in drinking water on risks of bone fractures. J Bone Miner Res.16(5):932-9.

12. Alarcon-Herrera MT et al. (2001). Well water fluoride, dental fluorosis, and bone fractures in the Guadaina Valley of Mexiico. Fluoride, 34(2) 138-48.

13. Strunecka A and Patocka J (1999). Pharmacological and toxicological effects of aluminofluoride complexes. Fluoride, 32, 230-242.

14. Varner JA et al. (1998). Chronic administration of aluminum-fluoride or sodium-fluoride to rats in drinking water: alterations in neuronal and cerebrovascular integrity. Brain Research, 784, 284-298.

15. Galletti P & Joyet G (1958). Effect of fluorine on thyroidal iodine metabolism in hyperthyroidism. Journal of Clinical Endocrinology; 18:1102-1110 http://www.fluoridealert.org/galletti.htm

16. Bachinskii PP et al. (1985) Action of the body fluorine of healthy persons and thyroidopathy patients on the function of hypophyseal-thyroid system. Probl Endokrinol (Mosk) 31(6):25-9.

16-A. Schlesinger ER et al .(1956). Newburgh-Kingston caries-fluorine study X111. Pediatric findings after ten years. Journal of the American Dental Association. V 52.

17. Connett E and Connett P (2002). Comments on Draft Toxicological Profile for Fluorides. Docket Control Number ATSDR-173. Submitted to: Division of Toxicology, Agency for Toxic Substances and Disease Registry, Mailstop E-29, 1600 Clifton Road, NE, Atlanta, Georgia 30333. (Available at: http://www.fluoridealert.org/pesticides/Fluorides.Comments.ATSDR.02.htm )

18. CDC (1999). Achievements in Public Health, 1900-1999: Fluoridation of Drinking Water to Prevent Dental Caries. Mortality and Morbidity Weekly Review (MMWR), 48(41);933-940 October 22, 1999.

19. CDC. (2001). Recommendations for Using Fluoride to Prevent and Control Dental Caries in the United States. Mortality and Morbidity Weekly Review. August 17, 50(RR14):1-42.

20. WHO Oral Health Country/Area Profile Programme. Department of Noncommunicable Diseases Surveillance/Oral Health. WHO Collaborating Centre, Malmö University, Sweden Available at: http://www.whocollab.od.mah.se/euro.html

21. Connett P and Connettt M (2000). The emperor has no clothes: a critique of the CDC’s promotion of fluoridation. Waste Not # 468; Oct 3. Waste Not, 82 Judson Street, Canton NY 13617. For a revised version of this article please see: http://www.fluoridealert.org/cdc.htm

22. DHHS (1991). Review of Fluoride: Benefits and Risks, Report of the Ad Hoc Committee on Fluoride of the Committee to Coordinate Environmental Health and Related Programs. Department of Health and Human Services, USA.

23. Heller KE et al (1997). Dental caries and dental fluorosis at varying water fluoride concentrations. J of Pub Health Dent, 57;No. 3, 136-143.

24. McDonagh MS (2000) Systematic review of water fluoridation. BMJ 2000;321:855-859 (7 October )

25. Fein NJ and Cerklewski FL (2001). Fluoride content of foods made with mechanically separated chicken. J Agric Food Chem. Sep;49(9):4284-6.

25-A. Lewis DW and Limeback H (1996). Comparison of recommended and actual mean intakes of fluoride by Canadians. Journal of the Canadian Dental Association; 62 (9): 708- 709 and 712-715. [Note: Table 16 can be found online at: http://www.gov.on.ca/MOH/english/pub/ministry/fluoridation/fluor.pdf ]

26. Li et al. (2001). Effect of long-term exposure to fluoride in drinking water on risks of bone fractures. J Bone Miner Res May;16(5):932-9.

27. Canada Report 1993. Priority Substances List Assessment Report. Inorganic Fluorides, Government of Canada, Environment Canada, Health Canada, Canadian Environmental Protection Act. ISBN 0-662-21070-9 Cat. No. En40-215/32E- Available at http://www.fluorideaction.org/pesticides/canada.1993.inorganic.f.pdf

28. Canada Report 1999. BENEFITS AND RISKS OF WATER FLUORIDATION. An Update of the 1996 Federal-Provincial Sub-committee Report. Prepared under contract for: Public Health Branch, Ontario Ministry of Health First Nations and Inuit Health Branch, Health Canada. Submitted by: Dr David Locker Community Dental Health Services Research Unit, Faculty of Dentistry, University of Toronto November 15, 1999.) Report can be downloaded from
Also at (scroll down for report): http://www.gov.on.ca/MOH/english/pub/ministry/fluoridation/fluoridation.html

29. Dyson Rose and John R. Marier (1977). Environmental fluoride 1977. National Research Council of Canada. NRC Associate Committee on Scientific Criteria for Environmental Quality. NRCC No. 16081. ISSN 0316-0114. http://www.fluorideaction.org/nrc-fluoride.htm

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Other comments submitted to US EPA on Dow’s petition for tolerances for Sulfuryl fluoride:

March 18, 2002. Comments submitted to EPA on DowAgroSciences petition to establish Fluoride and Sulfuryl fluoride tolerances for a large number (40) of raw and processed foods. Federal Register, February 15, 2002.

September 29, 2001. Comments submitted to US EPA from Ellen Connett on the Proposed Pesticide Temporary Tolerances that appeared in the September 5, 2001, Federal Register.