Fluoride Action Network
82 Judson Street, Canton NY
Email: pesticides@www.fluoridealert.org
http://www.fluoridealert.org/

July 5, 2011

To: U.S. EPA Office of Pesticides Programs

Comments on
Sulfuryl Fluoride; Proposed Order Granting Objections
to Tolerances and Denying Request for a Stay.
Federal Register, January 19, 2011
Docket ID: EPA-HQ-OPP-2005-0174; Document Number: 2011-917

FAN is responding to the EPA’s judgment on FAN’s interventions on the use of sulfuryl fluoride as a fumigant on food.

1. Whoever wrote this document should be congratulated for the clarity of their summation, especially their summary of the 8 years worth of submissions by FAN, Beyond Pesticides and the Environmental Working group.

2. The EPA has correctly summarized our “consolidated objections and hearing requests filed in November, 2006,” in which we raised six main arguments:

• The fluoride MCLG is not protective of the effects of fluoride on teeth and bones;
• The fluoride MCLG is not protective of other neurotoxic, endocrine, and renal effects of fluoride;
• EPA has not adequately protected children;
• EPA cannot determine the safety of sulfuryl fluoride and fluoride in the absence of a developmental neurotoxicity study
• EPA has underestimated exposure to fluoride; and
• EPA has committed procedural errors in violation of the Administrative Procedures Act (APA) (5 U.S.C. 551 et seq.)

3. We are happy that the EPA has accepted all these objections.

4. We also appreciate the arguments raised by the EPA for refusing our call for a stay of use of ProFume® based upon the fact that the EPA has announced a three year phase out of the use of sulfuryl fluoride as a fumigant on food. We agree that over the next three years other controllable sources of fluoride are of greater concern as far as exposure to fluoride is concerned –especially infants and young children. In this respect, we are extremely concerned about the continued promotion and protection of the use of artificial water fluoridation, the failure of government agencies to take aggressive steps to warn parents not to use fluoridated tap water to make infant formula, the failure of the CDC to warn vulnerable subsets of the population to the dangers posed to them by ingested fluoride, and the limited availability of non-fluoridated toothpaste for children under 7 years of age.

However, we would also raise a note of caution on the continued use of ProFume® over the next three years. While the impact of fluoride residues left in food averaged out over the average application rates may result in a relatively small average increment in increased fluoride exposure, this argument does not take into account FAN’s concerns with the possibility that fumigated food– eg, wheat flour at the permitted tolerance of 125 ppm – is distributed undiluted. If such flour in bread, pasta, cookies, cakes, or pizza, etc., was consumed by a child then it could cause acute toxic effects such as vomiting or worse. In addition, we are also concerned about the possibility of large batches of treated flour, or other foodstuffs fumigated with sulfuryl fluroide, when purchased by an institution (hospitals, universities, prisons, military establishments or for agencies distributing emergency rations). This too could lead to acute toxic effects in consumers. FAN requests the OPP to provide the specific steps that will be taken to avoid such situations and minimize potential acute effects.

5. We acknowledge the result of EPA’s calculations (but see comment in 12) that using the new proposed RfD from EPA’s Office of Water (OW) of 0.08 mg/kg/day, both with and without the use of sulfuryl fluoride, millions of children under 7 years of age are exceeding this RfD thus justifying EPA’s phase out sulfuryl fluoride as a food fumigant over the next three years.

6. However, we want to put on the record that we do NOT believe that this new RfD of 0.08 mg/kg/day is protective enough of infants and young children and we have raised objections to the OW’s over their derivation of this RfD (See attachments FAN 1, Dose; FAN 2, Sources; and the fluoride reports published since the publication of the NRC 2006 report at http://www.fluoridealert.org/since-nrc.html). We summarize these objections below (see 6 a-h)

7. The problems with OW’s derivation of the new RfD of 0.08 mg/kg/day:

• We believe that OW has corrupted the process of determining a MCLG that is SAFE because it has allowed considerations of the “presumed” benefits of water fluoridation to interfere. By announcing the need to protect the water fluoridation program and asserting an adequate intake for this purpose was 0.05 mg/kg/day, OW set an artificial upper limit level for a new MCLG, which skewered the way it went about choosing the most sensitive end point and the safety factors applied to this end point.

• We don’t think considerations of benefits should have been part of the process of setting standards for a “contaminant” especially since the EPA failed to examine the evidence of these purported benefits, which is very weak indeed. There have never been any double blind randomized clinical trials demonstrating that ingesting fluoride reduced tooth decay. In addition, the largest survey of dental decay among children in the U.S. found an average saving of less than one tooth surface out of 128 tooth surfaces in a child’s mouth attributable to water fluoridation, and even this was not shown to be statistically significant (Brunelle and Carlos, 1990). Such small differences could well be an artifact if fluoride caused a delayed eruption of the permanent teeth for which there is some evidence (Komarek et al, 2005). In the only study (the US government funded Iowa study) that has attempted to relate reduction in tooth decay to individual consumption of fluoride by children, no relation was found between tooth decay and the amount of ingested fluoride (Warren et al., 2009).

• We further reject the claim by OW and repeated by OPP the claim that fluoride is a nutrient (see the discussion in 9 below).

• We do not agree that severe dental fluorosis is the most sensitive end point of fluoride’s toxicity

• We believe that fluoride’s impact on the brain occurs at lower levels than those that the cause severe dental fluorosis. Unfortunately, the OW ignored our input on this issue, even though there have been many more IQ studies and other brain studies that have become available since NRC (2006) published its review 5 years ago. OPP acknowledges that we sent to the EPA pdf files of 18 of these studies. However, there has been several more brain studies since then: Ding et al., 2011; Valdez-Jiménez et al., 2011 (a review), and Pouresalmi et al. 2011 (an abstract). There have been at least 38 animal brain studies since the NRC report was published in March 2006 with only one, by Whitford et al. 2009, not finding an effect (see Brain: Animal Studies at end of references). A quick overview of the 25 IQ studies (the latest by Pouresalmi et al. in abstract only) (FAN 2011) indicates no support for the notion that a child has to have severe dental fluorosis before lowered IQ is observed.

• Even if OW had restricted itself to the end point of dental fluorosis we believe that the end point of concern should have been moderate dental fluorosis because of the evidence that this condition impact’s a child’s self esteem with resulting psychological stress. Dean’s definition of moderate dental fluorosis indicates that it impacts 100% of the enamel surface. It is hard to believe that any one could examine photos of so-called “moderate” dental fluorosis (as pictured below) and feel that a teenager’s self-esteem would not be impacted by such a condition.

Click here to see more photos of moderate dental fluorosis

In the NRC (2006) review the authors commented on the psychological impacts of moderate and severe dental fluorosis:

“The potential for psychological and behavioral problems to develop from the aesthetically displeasing consequences of enamel fluorosis has been a long-standing concern. In 1984, an ad hoc panel of behavioral scientists convened by the U.S. Environmental Protection Agency (EPA) and the National Institute of Mental Health to evaluate the issue concluded that “individuals who have suffered impaired dental appearance as a result of moderate and severe fluorosis are probably at increased risk for psychological and behavioral problems or difficulties” (R.E. Kleck, unpublished report, Nov. 17, 1984, as cited in 50 Fed. Reg. 20164 [1985]). The panel recommended research on the social, emotional, and behavioral effects of enamel fluorosis.” (p.119)

More recently an article published in the New York State Dental Journal in 2008, Elvir Dincer, DDS, concluded:

“that children’s self-esteem is harmed by even mild fluorosis.” (Dincer, 2008)

A recent review article by Chankanka et al., 2010, of 35 studies on this matter, while reporting mixed responses to the feelings about very mild and mild dental fluorosis, found little evidence of anything but a negative reaction by sufferers or observers to moderate dental fluorosis (Chankanka et al., 2010).

• Even if OW restricted itself to the end point of severe dental fluorosis, we believe that its application of an uncertainty factor of 1 to Dean’s data from 1942 (eliminating the normal safety factor of 10 for intra-species variation in sensitivity) was totally unjustified, because as OW itself acknowledged Dean did not look at a truly representative cross section of the US population of children. There were no black and Hispanic children in this study. Moreover, children from families from lower incomes were also under-represented. Using an uncertainty factor of 1 here is not only a violation of common sense and normal regulatory risk assessment procedures but is also tantamount to a violation of the principles of Environmental Justice espoused by the EPA (see further discussion in 9) below).

• Another reason to be very cautious about the RfD of 0.08 mg/kg/day is that OW has yet to review the evidence that fluoride may cause osteosarcoma in young men. Since Bassin et al. (2006) published their osteosarcoma findings of an age- and sex-specific effect from exposure to fluoride there has been no study published since to refute it. It has been over five years since such a refutation was promised by Bassin’s thesis advisor, Chester Douglass, in a letter to the journal Cancer Causes and Control (Douglass and Joshipura, 2006). How long is OW going to leave this issue in limbo? At the very least, the EPA should carefully examine Douglass’s methodology to see if it has ability to refute Bassin’s findings. If as reported it is based on an assessment of bone levels at diagnosis or autopsy it simply is not sufficient to challenge Bassin’s central thesis of a 5-7 fold increased risk of osteosarcoma for young boys by age of 20, when exposed at the ages of 6-8 years, since bone levels are cumulative and cannot be used to predict exposure during this critical age range.

8. Any future amelioration of the RfD determination that recognizes any or all of our objections 6 a-g above, could only lower the MCLG from 0.08 mg/kg/day and thus would not change the OPP’s conclusions that millions of children under 7 years of age are already exceeding the MCLG. In other words no lowering of the MCLG would negate OPP’s recognition that its legally bound not to allow any increased burden to these infants or children with the use of sulfuryl fluoride on food or any other fluoride-generating pesticide that adds fluoride to the human food chain.

9. Because of the OW’s failure to do an appropriate determination of the MCLG as outlined above (6 a-g), we urge OPP, when doing any future risk assessments on the fluoride left over from other pesticides that they not defer to OW’s calculations determined under SWDA requirements but to do their own risk assessments taking into full account the special extra safety requirements to protect infants and young children provided under the Food Quality Protection Act of 1996 (FQPA) and incorporated in FFDCA.

10. FAN rejects OPP’s analysis in section 3, that deals with the OW’s choice of an uncertainty factor of 1 in extrapolating from Dean’s data from 1942, and states:

“3. Children’s safety factor. In choosing a revised RfD for fluoride, OW did not apply any uncertainty or safety factors to the BMDL for severe dental fluorosis. OW reasoned that uncertainty factors were not warranted due to the extensive human epidemiological data on the effects of fluoride, including extensive data on children, the population of greatest concern. Decisions on pesticide tolerances, however, require OPP to apply special provisions for protection of children. Specifically, section 408(b)(2)(C) of FFDCA provides that EPA shall apply an additional tenfold (10X) margin of safety for infants and children in the case of threshold effects to account for prenatal and postnatal toxicity and the completeness of the database on toxicity and exposure unless EPA determines based on reliable data that a different margin of safety will be safe for infants and children. In making determinations on this children’s safety factor, OPP has focused on the statutory factors of data completeness with regard to toxicity and exposure and evidence bearing on pre- and post-natal toxicity.”

FAN reiterates that the intra-species factor should not have been dropped because Dean’s study from 1942 did not cover a full cross-section of the U.S. population. Moreover, while a case might be made for dropping the requirement for an extra safety factor for prenatal and postnatal toxicity in the very limited case of dental fluorosis it would be totally unjustified if OW and OPP chose a more realistic end point of damage to neurodevelopment. FAN presented ample evidence for both fluoride’s prenatal and postnatal effects on the brain.

This latter point also further underlines another of FAN’s objections, namely that no neurodevelopmental studies have been done on sulfuryl fluoride as required by FFDCA. This further underlines the dangers of using a risk assessment supposedly done to meet the more limited requirements of SWDA and applying it a risk assessment to meet the more stringent requirements of FFDCA.

11. FAN rejects the claim by OW and repeated by OPP that fluoride is a nutrient. Fluoride is not a nutrient (Alberts & Shine 1999; NRC 1993), nor is it essential for healthy teeth. No study has ever revealed a diseased state resulting from lack of fluoride, including dental caries. No American is, or ever was, “fluoride deficient.”
To demonstrate a substance is an essential nutrient it is necessary to starve an animal of the substance in its diet and demonstrate that some disease accrues. This has never been done for fluoride for either tooth decay or for anything more serious.

Thus FAN rejects OPP’s analysis which attempts to use the false claim that fluoride is a nutrient for eliminating the requirement under FFDCA to apply an extra safety factor in risk assessment to protect children from their presumed extra sensitivity to pre-natal and post-natal toxicity in section 3. c

“c. Pre- and post-natal toxicity. Not only does OPP have extensive data identifying fluoride’s effects in humans and the dose at which those effects occur, but fluoride, unlike most pesticides or their metabolites, is considered a human nutrient. Fluoride’s classification as a nutrient—especially its role at certain doses in protecting teeth—cannot be ignored in the safety factor calculation. OPP is averse to choosing a safety factor that would result in the choice of a PAD that indicates that fluoride is harmful at levels below the adequate intake level for beneficial effects. The Objectors have raised concerns about potential other effects of fluoride—for example, brain, endocrine, kidney, and reproductive effects. Nonetheless, data on these effects generally either shows effects only at considerably higher levels than the levels causing severe dental fluorosis or are very equivocal.

“On balance, the extensiveness of the data on toxicity of fluoride and human exposure to it, the clear data defining the safe level for the effect of concern on children, and fluoride’s status as a human nutrient at levels only slightly below the level that is protective against severe dental fluorosis lead OPP to conclude that reliable data show that an additional safety factor for the protection of children is not necessary. Accordingly, OPP has not used an additional safety factor in its fluoride risk assessment. Hence, the PAD for fluoride is equivalent to the RfD (0.08 mg/kg/day). (Ref. 23 at 9). (our emphasis)”

FAN rejects this analysis on several grounds.

a) OPP offers no evidence that fluoride is a nutrient (see the discussion above)

b) OPP while claiming it has “extensive data identifying fluoride’s effects in humans” has actually ignored a very critical part of the data base on fluoride’s effects on humans – namely fluoride’s impact on the developing brain, for which FAN provided them with a extensive bibliography and commentary. This problem is further compounded by the failure of Dow to provide neurodevelopmental studies on sulfuryl fluoride.

c) When OPP states that “Fluoride’s classification as a nutrient—especially its role at certain doses in protecting teeth—cannot be ignored in the safety factor calculation.” We argue to the contrary: fluoride’s presumed nutritional benefits MUST be ignored, if the task at hand is to determine levels of fluoride that are deemed safe to protect the population from harm. This determination should not be corrupted by a poorly defended administrative need to protect the water fluoridation program (as discussed above).

12. FAN does not agree with EPA when it states,

“EPA also has an extensive set of animal data on sulfuryl fluoride and to the extent that sulfuryl fluoride breaks down to the fluoride anion during testing… OPP concludes that the completeness of the database with regard to fluoride exceeds what is generally available even on the most well-studied pesticides.”

The key studies required by FFDCA have yet to be performed by Dow, especially the neurodevelopmental studies, which FAN has requested several times. Moreover, the numerous animal studies performed by Dow on sulfuryl fluoride provided few details of the effects on bone, aside from a micronucleus assay in mouse bone marrow cells. No fluoride levels in bone were measured in any sulfuryl fluoride study. Also, since Bassin et al. published their osteosarcoma findings of an age- and sex-specific effect from exposure to fluoride there has been no study published since to refute it. There is a great need to proceed with caution when the carcinogenicity of fluoride remains unresolved.

13. FAN has yet to do an in-depth check of the assumptions and calculations leading to the tables in this report, We reserve our judgment on these. They may become an issue when the OW moves from the RfD (and hopefully a more scientifically defendable RfD) to an MCLG.

14. Lastly, we disagree with OPP for excluding ambient air exposures as a source of fluoride exposure in it’s aggregate assessment:

“g. Other sources of fluoride exposure. Although people are also potentially exposed to fluoride from fluoride in ambient air, fluoride dental treatments, and pharmaceuticals, among other things, OW concluded that these sources of exposure are insignificant compared to other sources of fluoride exposure. Accordingly, OPP is not including such exposures in its aggregate assessment. (Ref. 23 at 16).”

Fluoride is persistent and will not degrade in the environment or in the human body, where it has a very long half-life, estimated at 20 years (NRC, 2006; page 92). According to the 2008 Toxic Release Inventory (TRI) over 68 million pounds of fluoride chemicals (Hydrogen fluoride, Fluorine, Sulfuryl fluoride) were released in 2008. The majority of these releases, nearly 51 million pounds, are from coal-fired electric utilities.

While EPA approves and regulates fluoride-emitting industries, the public is not aware of any monitoring that is performed to determine the fate of these releases, or if levels in humans or the environment are being collected, particularly in fluoride-emitting industrial communities. According to TRI, the reported emission releases for these fluoride chemicals from 1998 to 2008 was over 780 million pounds.

1998-2008 – TRI Data for Hydrogen Fluoride and Fluorine Emissions
Year	Hydrogen Fluoride Releases INDUSTRY	Fluorine Releases INDUSTRY	Hydrogen Fluoride Releases FEDERAL FACILITY	Fluorine Releases FEDERAL FACILITY
2008	64,972,078	91,874	3,101,106	20
2007	74,016,222	173,364	3,233,252	16,926
2006	74,869,865	121,485	3,387,316	17,458
2005	76,801,757	98,788	3,503,879	None listed
2004	76,625,243	107,381	3,361,829	None listed
2003	74,496,396	83,923	3,585,055	None listed
2002	75,915,082	159,333	3,560,218	None listed
2001	72,138,405	165,946	2,176,817	None listed
2000	76,852,488	224,003	2,084,242	None listed
1999	77,402,530	246,557	1,956,305	None listed
1998	83,229,929	261,655	2,140,805	None listed
* 1998 was the first reporting year for electric utilities (the major source of Hydrogen Fluoride emissions), hazardous waste management facilities (a large source for Hydrogen Fluroide emissions) and other categories.
1997	13,703,681	84,291	3,259	None listed

TRI began reporting data on sulfiuryl fluoride in 1995. From 1995-2008, nearly 4 millions pounds have been released to the environment.

Sulfuryl Fluoride Releases: 1995 – 2008
2008 – 109,865	2005 – 84,086	2002 – 218,500	1999 – 525,000	1996 – 362,000
2007 – 112,245	2004 – 142,720	2001 – 215,000	1998 – 466,000	1995 – 355,007
2006 – 85,571	2003 – 224,258	2000 – 635,000	1997 – 428,000

We do have one example of the fluoride levels in soil and in foliage from industrial activity. At a site approximately seven miles from the aluminum smelters in Massena NY, the Ontario Ministry of Environment (MOE, 1999) performed an analysis of fluoride on 28 soil and 30 foliage samples in Cornwall, Ontario, Canada. All soil samples significantly exceeded the MOE’s Guidelines for Use at Contaminated Sites in Ontario. Of the 30 foliage samples, 27 exceeded the MOE’s Upper Limits of Normal contaminant guidelines. While the soil levels represent deposition over decades, the foliage samples represent approximately six months of exposure to air-borne fluoride (MOE, 1999). While these elevated levels are not a surprise, the communities who live in the shadow of these industries, or down wind, have never been informed of potential exposures, especially for hand-to-mouth exposure of young children playing outdoors. These may well be significant exposures for thousands of Americans when you add in the states ranked by TRI for hydrogen fluoride releases in 2008 at http://www.fluoridealert.org/tri-2008.pdf . The state of Ohio is ranked number one with 9,115,568 millions pounds released in 2008.

Sincerely,
Paul Connett, PhD
Director, Fluoride Action Network

References:

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Bassin EB, et al. 2006. Age-specific fluoride exposure in drinking water and osteosarcoma (United States). Cancer Causes and Control 17: 421-8.

Brunelle JA, Carlos JP. 1990. Recent trends in dental caries in U.S. children and the effect of water fluoridation. J. Dent. Res 69, (Special edition), 723-727.http://www.fluoridealert.org/health/teeth/caries/nidr-dmfs.html

Chankanka O, et al. 2010. A literature review of aesthetic perceptions of dental fluorosis and relationships with psychosocial aspects/oral health-related quality of life. Community Dent Oral Epidemiol. Apr;38(2):97-109.

Dincer E. 2008. Why do I have white spots on my front teeth? N Y State Dent J. Jan;74(1):58-60.

Ding et al., 2011. The relationships between low levels of urine fluoride on children’s intelligence, dental fluorosis in endemic fluorosis areas in Hulunbuir, Inner Mongolia, China. Journal of Hazardous Materials 186:1942–1946.

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Brain: Animal Studies from since the NRC report was published in March 2006.

See all the brain studies at http://www.fluoridealert.org/since-nrc.html

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Full report

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Full Report