Fluoride Action Network

Cryolite: FAN Comments submitted to EPA in May 2002

August 20th, 2012

Cryolite

May 24, 2002, comments submitted to EPA on
Gowan Company’s petition for new, modified, and proposed tolerances,
(Federal Register, April 24, 2002).
US EPA Docket control number OPP-2002-0007.

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

Submitted via Email, Fri, 24 May 2002 22:08:04 -0400
To: opp-docket@epa.gov

Gowan’s petition: Specific actions requested. Federal Register, April 24, 2002.
Modify existing tolerances:
Apricots from 7 ppm to 10 ppm
Cucumber from 7 ppm to 4 ppm
Cranberry from 7 ppm to 2 ppm
Kale from 7 ppm to 35 ppm
Kiwi from 15 ppm to 8 ppm
Nectarines from 7 ppm to 10 ppm
Plums from 7 ppm to 2 ppm (tolerance with regional registration)
Renew tolerances and remove time-limitation:

Potatoes – 2 ppm

Potatoes, waste from processing – 22 ppm

Establish new tolerances:

Berries (crop group 13) – 0.5 ppm
replaces separate existing tolerances for
blackberries, blueberries, boysenberries, dewberries, loganberries, raspberries and youngberries

Prunes – 7 ppm (tolerance with regional registration)

May 24, 2002

Docket control number OPP-2002-0007

We submit the following comments in response to Gowan’s proposed, new, and modified tolerances published in the Federal Register on April 24, 2002 – Docket control number OPP-2002-0007. Our comments are also available online at http://www.fluoridealert.org/pesticides/Cryolite.Comments.May24.02.htm — We urge the EPA to implement online accessibility to all comments and documents that have the potential to influence their decisions and those of the public regarding pesticides.

1. Gowan’s petition states:

EPA concluded in the cryolite RED, that the NTP studies utilizing sodium fluoride in lieu of cryolite satisfy the guideline study requirements for both the rodent chronic feeding study and the rat carcinogenicity study.

1.1 When the EPA treats cryolite simply as a source of fluoride they oversimplify the chemistry. In addition to fluoride there will be free aluminum ions present or intermediate aluminum-fluoride complexes. There are several lines of scientific evidence to suggest that fluoride in the presence of aluminum is a far greater concern than fluoride alone. In this respect one key experiment was conducted by Varner et al. (1998) which showed greater impacts on the brain with rats treated with aluminum fluoride at 1 ppm fluoride than sodium fluoride at 1 ppm fluoride. This study is discussed elsewhere in this critique.

1.2 There are several experiments reported in the literature where fluoride in the presence of a trace amount of aluminum triggers the G-protein messenger transmission system for water soluble hormones, neural transmitters, and certain growth factors. This is potentially extremely serious and is discussed elsewhere in this critique.

2. Gowan’s petition states

… the Agency has determined that although, fluoride accumulation is demonstrated in a number of studies, the accumulation itself is not considered an adverse effect.

2.1 Anything that accumulates in the human body is potentially dangerous. This is why the body has mechanisms to get rid of fat soluble toxins otherwise they accumulate in fat. And that is why water soluble substances like fluoride are excreted through the kidney. However, it’s generally accepted that 50% of the fluoride (for healthy people under fifty years of age -ATSDR, 1993, p 112) is not excreted and accumulates in the bone. It would be reckless to assume that fluoride accumulation from ALL sources that we are exposed to including pesticide residues will not cause deleterious effects on the bone and the pineal gland.

2.2 Until Jennifer Luke’s work (1997, 2001) many people were unaware that the pineal gland produced the same crystals of calcium hydroxy apatite as the bones and teeth. It is shocking that no U.S. agency has yet to address Luke’s studies in any public statement or peer reviewed document.

2.3 Luke’s work is particularly illuminating in this respect because not only did she show that fluoride accumulated in the human pineal gland but she also showed that it lowered the production of melatonin in animal studies, the hormone that is produced in this gland.

2.4 Luke also noted a finding from the first 10-year follow-up health study of 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 (Schlesinger et al., 1956). 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.

2.5 The Cryolite RED (US EPA, 1996) document noted that in the majority (if not all) studies at all exposure levels fluoride was found to accumulate. The Maximum Contaminant Level for fluoride of 4 ppm in U.S. drinking water was based on crippling skeletal fluorosis as the adverse impact. There are several painful adverse health conditions that precede skeletal fluorosis as noted in a Canadian report (1993, p 29):

Clinical signs associated with the preclinical and (3) clinical stages of skeletal fluorosis have been reviewed (U.S. DHHS, 1991), with the severity of this condition related to the amount of fluoride in the bone. In the preclinical phase, the “fluorotic” patient may be relatively asymptomatic, with only a slight increase in bone mass (detected radiographically) [however, the diagnosis of (early-stage) skeletal fluorosis may differ among health care professionals (Chan-Yeung et al., 1983a)]. Sporadic pain and stiffness of the joints, chronic joint pain, osteosclerosis of cancellous bone, and calcification of ligaments are associated with the first and second clinical stages of skeletal fluorosis… While bone without fluoride-induced alterations contains approximately 500 to 1,000 mg fluoride/kg bone (ash weight), the concentration of fluoride in the bone of individuals with the preclinical or crippling stages of skeletal fluorosis may be between 3,500 and 5,500 or greater than 8,400 mg fluoride/kg bone, respectively (U.S. DHHS, 1991). A number of factors such as age, nutritional status, renal function, and calcium intake, in addition to the extent and duration of exposure can influence the amount of fluoride deposited in bone, and, consequently the development of skeletal fluorosis (U.S. DHHS, 1991). Individuals with impaired renal function (such as those with diabetes) may be more prone to developing fluoride-related toxicological effects (i.e., fluorosis) due to their diminished excretion of fluoride (ATSDR, 1991 [sic: 1993]; U.S. DHHS, 1991; Kaminsky et al., 1990; WHO, 1984).

2.6 The accumulation of fluoride in the bone has been shown to cause bones to become more brittle and subject to fracture. In this respect the study by Li et al. (2001) is particularly striking because a simple doubling of the fluoride concentration doubled the rate of hip fracture in the elderly and quadrupling the concentration in the drinking water caused a tripling of hip fracture rates in the elderly. 2.7 To add another level of seriousness to this analysis, a study conducted by Alarcon-Herrera (2001) 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.

2.7 Another note on accumulation: Studies cited in a Canadian report (1993):

Limited available evidence indicates that biomagnification of inorganic fluoride does not occur in aquatic or terrestrial food chains (ATSDR, 1991 [sic: 1993]); however, some aquatic and terrestrial biota bioaccumulate soluble inorganic fluorides (Hemens and Warwick, 1972; Barbaro et al., 1981; ATSDR, 1991 [sic: 1993]). In samples obtained near a reclaimed fluorspar-mining site, the levels of inorganic fluorides in plants, invertebrates, and small mammals were higher than those in samples obtained from a control site (Andrews et al., 1982). Twenty-four hours after sodium fluoride was released into an experimental pond, the concentration of fluoride in aquatic vascular plants was increased 35-fold, and uptake was also increased in algae (14-fold), mollusks (12-fold), and fish (7-fold) [Kudo and Garrec, 1983].

3 Gowan’s petition states:

EPA has determined that the dose to be used for risk assessment for exposure to fluoride is 0.114 mg F/kg/day, per the 1996 Cryolite RED. This value is used for all population subgroups, and is derived from a maximum acceptable amount of fluoride in drinking water recommended to the EPA by the Surgeon General as providing an adequate margin of safety for avoiding skeletal fluorosis (1996 Cryolite RED).

3.1 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). The Department of Health and Human Services (DHHS, 1991) 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 the food commodities in Gowan’s petition to the high end of this range and reported how close – how very close- this is to the MCLG.

3.2 The situation is even worse for children. The same DHHS study cited above (DHHS, 1991) 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.

3.3 The over exposure of our children to fluoride is also disturbingly confirmed by the dental fluorosis rates. In a study by Heller et al (1997), 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 (McDonagh, 2000) 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.

3.4 According to a Canada report (1993):

The total average daily intake of inorganic fluoride via ingestion by exclusively breast-fed infants was estimated to range from approximately 0.5 to 2.6 mg/kg bw/day, while the intake in exclusively formula-fed infants was estimated to range from 13.6 to 93.0 mg/kg bw/day.

3.5 Fein and Cerklewski (2001) reported on high fluoride content of certain children’s foods made with mechanically deboned chicken. They state:

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.

3.6 At least twelve years ago dental products that contain fluoride, such as toothpaste, were identified as significant sources of inorganic fluoride for children and adolescents (Drummond et al., 1990).

3.7 Lewis and Limeback (1996) found that children up to 11 years of age in North America are being over-exposed to fluoride.

3.8 The average American is already close to the MCLG discussed above. Under these circumstances it is irresponsible to conduct an analysis by comparing the incremental dose of the tolerances in this petition 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.

3.9 Some other routes of exposure not accounted for. Rose and Marier (1977) cited a 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.

3.10 The US EPA needs to recalculate an up-to-date estimate of the daily dose of fluoride for infants, children and adults. It needs to add the estimated increment from increased fluoride residue exposure to the high end user and to the background exposure doses to infants and adults for the new, proposed and modified tolerances petitioned for by Gowan.

4 In a long-term, low-dose rat fluoride study Varner et al. (1998) 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 an indicator for Alzheimer’s Disease. The authors speculate that fluoride facilitates aluminum to cross the blood brain barrier.

4.1 In EPA’s September 5, 2001 (Federal Register) risk assessment of fluoride they found that the majority of adverse effects from animal studies affected the brain.

4.2 A serious omission in Gowan’s petition is the lack of reference to EPA’s updated risk assessment for fluoride (Federal Register, September 5, 2001). Gowan’s petition for proposed, new, and modified tolerances are premature until studies are performed to assess cryolite’s effect on the brain, particularly the white matter. The risks associated with damage to the brain white matter is of critical importance to all age groups. For example, EPA reported the following (Federal Register, September 5, 2001):

4.2.1) In a 2-generation reproduction inhalation study in rats, vacuolation of the white matter in the brain… were observed in the parental animals.

4.2.2) 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.

4.2.3) 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.

4.2.4) 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)…

4.2.5) 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

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

4.2.7) In a 90-day study (rat)… Vacuolation of the white matter in the cerebrum was also observed at 300 ppm in this study.

4.3 Since the middle 1990s there have been several important studies which have probed fluoride’s possible impact on the brain. Mullenix et al. (1995) demonstrated that rats treated prenatally with fluoride showed behavior patterns associated with hyperactivity and rats dosed after birth showed hypoactivity. Guan et al. (1998) showed that membrane lipids in rat brain were impacted by chronic fluorosis. Guan’s group found that several key chemicals in the brain – those that form the membrane of brain cells – were substantially depleted in rats given fluoride, as compared to those who did not get fluoride.

4.4 Several studies in China (Li 1995; Zhao et al. 1996; and Lu et al. 2000) have shown the possible impact of high background fluoride (possibly in the presence of low iodide, Zhao, 1998) on children’s IQ. One of those that we have examined is the work by Zhao et al (1996) who found an approximate 5-10 point IQ deficit in children from a community with water containing 4 ppm natural fluoride compared to one containing 1 ppm. Since we fluoridate at 1 ppm, and the EPA’s MCLG for fluoride is 4 ppm, this paper is of considerable concern.

4.5 According to Christopher Filley (2001):

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. (p 3-4)… Early clinical features of cerebral white matter involvement typically include confusion, inattention, memory dysfunction, and personality changeÉ Measures of attention, cognitive speed, memory retrieval, visuopatial skills, and executive function are likely to be most sensitive to subtle white matter dysfunction (p 249)… (Our emphasis.)

4.6 This is 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 (1999). This is another huge important area ignored by the US EPA.

4.7 The fluoride study by Mullenix et al. (1995) found that fluoride was taken up in the brain and had adverse effects on rat behavior. 4.8 A Canadian report (1993) noted:

In a number of analytical epidemiological studies, an increased incidence of lung and bladder cancer and increased mortality due to cancer of the lung, liver, bladder, stomach and oesophagus, pancreas, lymphatic-hematopoetic system, and brain (central nervous system) was observed in workers employed in the aluminum smelting industry (using cryolite as a source of aluminum) [reviewed in Ronneberg and Langmark, 1992]; however, generally there has been no consistent pattern (bone cancer was not usually assessed) (page 28).

5 Cryolite is applied by aerial equipment and ground sprayers up to several times per season (US EPA Cryolite RED, page 17). There is no mention or assessment of the potential for exposures to aerial drift from cryolite application. This assessment should have been conducted prior to Gowan’s petition to allow the public to assess the risks involved. If an assessment for this exposure was done it should have been included in Gowan’s petition.

5.1 Gowan is negligent for not including EPA’s September 5, 2001, risk assessment for fluoride which included inhalation studies as Cryolite is applied by aerial equipment and ground sprayers (EPA Cryolite RED, page 17).

5.2 Is it the responsibility of EPA to insure the safety of farm workers exposed to spray applications of Cryolite via an assessment of the exposure risks involved? Has an assessment for their exposure been considered in light of EPA’s September 5, 2001, updated risk assessment for fluoride? How are farm workers and area residents who could be potentially exposed by aerial spray drift to know the risks? The public should be made aware of the risks.

6. Reproductive toxicity: A 1993 Canadian report cited the following:

6.1 “Adverse effects on reproductive function have been observed in female mice administered (orally) * 5.2 mg/kg bw/day fluoride on days 6 to 15 after mating (Pillai et al., 1989), and in male rabbits administered (orally) * 9.1 mg/kg bw/day fluoride for 30 days (Chinoy et al., 1991). Histopathological changes within the organs of the reproductive system have been observed in the testes of male rabbits administered (orally) 4.5 mg/kg bw/day fluoride for 18 to 29 months (Susheela and Kumar, 1991), in the ovaries of female rabbits injected subcutaneously with * 10 mg/kg bw/day fluoride for 100 days (Shashi, 1990), and in the testes of male mice administered (orally) * 4.5 mg/kg bw/day fluoride for 30 days (Chinoy and Sequeira, 1989a, 1989b) (Page 26 of Canadian Report).”

6.2 “Alterations in the lipid content of the lung, thyroid, and testis (Shashi, 1988, 1992; Shashi et al., 1987, 1989), muscle fibre hypertrophy and necrosis (Shashi, 1989), and reduced protein (acidic and basic) content of the thigh muscle (Shashi et al., 1992) were observed in animals receiving * 2.3 mg/kg bw/day fluoride, compared to controls (Page 21 of Canadian Report).”

7.0 Gowan’s petition to remove time-limits on tolerances for Potatoes at 2 ppm and Potato processing waste at 22 ppm is premature. The public need to know the results of this experiment. For example, what are the levels in the meat, milk, and meat-by products in the animals fed the potato waste with fluoride levels of 22 ppm.

8.0 Kale (proposed tolerance 35 ppm), Prunes (proposed tolerance7 ppm), and the tolerances for all other food commodities: Was the bioaccumulation of fluoride in processing in fluorinated water taken into account in the assessment of fluoride exposure for all age groups?

References:
Note: Italicized references are those cited in the Canada (1993) report.

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. Available online: http://www.fluoride-journal.com/01-34-2/342-139.pdf

Andrews, S.M., J.A. Cooke, and M.S. Johnson. 1982. Fluoride in small mammals and their potential food sources in contaminated grasslands. Fluoride 15: 56Ð63.

ATSDR (1993). Toxicological profile for fluorides, hydrogen fluoride, and fluorine (F). U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry. TP-91/17.  (Note: “People over the age of 50 often have decreased renal clearance[of fluoride] (p 112).”

Barbaro, A., A. Francescon, and B. Polo. 1981. Fluoride distribution along chlorinity gradients in Baltic Sea waters. Finn. Mar. Res. 248: 129Ð136.

Canada (1993). Inorganic Fluorides. Canadian Environmental Protection Act. (Priority Substances List Assessment Report.) Government of Canada, Environment Canada, Health Canada. ISBN 0-662-21070-9.
Cat. No. En40-215/32E.

Chan-Yeung, M., R. Wong, D. Enarson, M. Schulzer, K. Subbarao, J. Knickerbocker, and S. Grzybowski. 1983a. Epidemiological health study of workers in an aluminum smelter in Kitimat, B.C. II. Effects on musculoskeletal and other systems. Arch. Environ. Health 38: 34Ð40.

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.

Drummond BK et al. (1990). Estimation of fluoride absorption from swallowed fluoride toothpastes. Caries Res. 24: 211-215.

Federal Register. September 5, 2001. Sulfuryl Fluoride; Proposed Pesticide Temporary Tolerances. Volume 66, Number 172, Page 46415-46425. 40 CFR Part 180 [OPP-301166; FRL-6799-6] RIN 2070-AC18. Available online: http://www.epa.gov/fedrgstr/EPA-PEST/2001/September/Day-05/p22283.htm

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

Filley C (2001). The Behavioral Neurology of White Matter. Oxford University Press, 2001.

Guan ZZ et al. (1998). Influence of chronic fluorosis on membrane lipids in rat brain. Neurotoxicology and Teratology 20 537-542.

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.

Hemens, J. and R.J. Warwick. 1972. The effects of fluoride on estaurine organisms. Water Res. 6: 1301Ð1308.

Kaminsky, L.S., M.C. Mahoney, J. Leach, J. Melius, and M.J. Miller. 1990. Fluoride: Benefits and risks of exposure. Crit. Rev. Oral Biol. Med. 1: 261Ð281.

Kudo, A., and J.-P. Garrec. 1983. Accidental release of fluoride into experimental pond and accumulation in sediments, plants, algae, molluscs and fish. Regulatory Toxicology and Pharmacology 3: 189Ð198.

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. Table 16: Recommended and actual fluoride intake estimates. Table 16 is available online at: http://www.gov.on.ca/MOH/english/pub/ministry/fluoridation/fluor.pdf

Li, XS (1995). Effect of Fluoride Exposure on Intelligence in Children. Fluoride, 28:4, 189-192.

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.

Lu Y et al. (2000). Effect of high-fluoride water on intelligence of children. Fluoride, 33:2, 74-78. Available online: http://www.fluoride-journal.com/00-33-2/332-74.pdf

Luke, J (1997). The Effect of Fluoride on the Physiology of the Pineal Gland. Ph.D. Thesis. University of Surrey, Guildord, U.K. (Note: A copy of this thesis was sent to Dennis McNeilly at US EPA Registration Division (7505C), in November -possibly October- 2001 by Ellen Connett. It is long document and the postage cost was high. We suggest that those who wish to review this thesis request it from McNeilly –(703) 308-6742. However, if it is unavailable at EPA’s office please contact us and we will send another copy.)

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

McDonagh MS (2000) Systematic review of water fluoridation. BMJ 2000;321:855-859 (7 October ). Online at: http://bmj.com/cgi/reprint/321/7265/855.pdf

Mullenix PJ et al. (1995). Neurotoxiicty of sodium fluoride in rats. Neurotoxicology and Teratology.17:2, 169-177.

Ronneberg, A., and F. Langmark. 1992. Epidemiologic evidence of cancer in aluminum reduction plant workers. Am. J. Ind. Med. 22: 573Ð590.

Rose D and Marier JR (1977). Environmental fluoride 1977. National Research Council of Canada. NRC Associate Committee on Scientific Criteria for Environmental Quality. NRCC No. 16081. ISSN 0316-0114.

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

Strunecka A and Patocka J (1999). Pharmacological and toxicological effects of aluminofluoride complexes. Fluoride, 32:4, 230-242.

US EPA (1996). Reregistration Eligibility Decision (RED) Cryolite. Report No. EPA-738-R-96-016.

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.

WHO (World Health Organization). 1984. Fluorine and Fluorides. Environmental Health Criteria 36. World Health Organization, Finland. 136 pp.

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

Zhao W (1998). Long-term effects of various iodine and fluorine doses on the thyroid and fluorosis in mice. Endocr Regul 32(2):63-70.

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NOTE:
We sent the following email to EPA <opp-docket@epa.gov>. The above submission is the corrected version.

May 25, 2002

Docket control number OPP-2002-0007

ADDENDUM TO COMMENT SUBMITTED:

We wish to make the following changes to our submission.

3.1 Last sentence. Changes are in CAPS: “A conservative assessment would have added the incremental dose predicted from a high use consumer of THE FOOD COMMODITIES IN GOWAN’S PETITION to the high end of this range and reported how close – how very close- this is to the MCLG.
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4.4 should read: “Several studies in China (Li, 1995 — NOT Lee et al. 1985)
The reference is: Li, XS (1995). Effect of Fluoride Exposure on Intelligence in Children. Fluoride, 28:4, 189-192.
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4.7 should read: “The fluoride study by Mullenix et al. (1995) (we left out the year)
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We used several citations from a report we called “Canada report (1993).” We added the references (in italics) cited in this report for convenience. One of the references cited the ATSDR 1993 toxicological profile for fluoride as “ATSDR, 1991”. We noted the error in each case.
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In the following email I will send the corrected version. It is also available online at: http://www.fluoridealert.org/pesticides/Cryolite.Comments.May24.02.htm

Note: In sending our corrected version to EPA we noted that if it was unacceptable because the deadline was May 24, then our May 24th version was our “official” submission.