Dr. Sauerheber’s 17th Letter to FDA

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Letter 17 to FDA

Cardiovascular Disease – Selmer Tennessee – EPA vs. FDA as Responsible for Fluoridation

Richard D. Sauerheber, Ph.D.
Palomar Community College
1140 W. Mission Rd., San Marcos, CA 92069
E-mail: richsauerheb@hotmail.com   Phone: 760-402-1173

February 10, 2012

Department of Health and Human Services
Public Health Service
U.S. Food and Drug Administration
Center for Drug Evaluation and Research
Office of Regulatory Policy
Rockville, MD 20857

Dear FDA Project Reviewers,

I write this letter in support of my previous petition to ban the addition of synthetic industrial fluoride compounds into public drinking water supplies, original petition FDA-2007-P-0346, formerly 2007P-0400.  The letter contains three principle sections: I. Cardiovascular effects of ingested industrial fluorides and the recent data for the Veterans’ Administration Healthcare System, Los Angeles indicating fluoride preferentially incorporates into atherosclerotic plaque and diseased heart tissue. II. A discussion of the withdrawal of a fluosilicic acid chemical supplier from the city of Selmer, Tennessee that could not provide data demonstrating either caries reduction or safety of use in the infirmed for consumers who ingest the chemical they provided. III. Direct communications with the U.S. EPA Office of Drinking Water, Region 9, San Francisco proving that EPA has no intention of regulating the procedures or chemicals used to treat humans with industrial fluoride compounds to be taken internally through public water supplies, which confirms the Petition for Reconsideration 2010 that the FDA, not the EPA, is exclusively in charge of regulating/prohibiting the dissemination of fluoride compounds to be taken internally through ingestion by citizens in the U.S.

I. Cardiovascular Effects of Systemic Industrial Fluoride.
The National Research Council 2006 Report [1] avoided discussion of the effects of industrial fluoride ingestion on cardiovascular function because comparatively so much more data existed for review on other organ systems (personal communication with Dr. K. Thiessen, coauthor of NRC Report). This is most unfortunate, since the mechanism of acute high level fluoride toxicity is known to be heart block due to inhibition of calcium ion mobility and related sequelae [2], the cause of death in the Nation’s worst water fluoride disaster in Hooper Bay, Alaska (see original petition). Further, at lower, intermediate blood levels of fluoride, research animals during long-term consumption develop heart muscle degradation and weakening [3]. Finally, for ‘low’ fluoride levels in consumers in U.S. treated cities, 0.2 ppm in blood, it has been long known that heart attack incidence increases in fluoridated cities. In Newburg, N.Y., heart attack incidence increased 1.7 fold after fluoridation began, which exceed the National average for the first time in city history, far in excess of incidence in the control city of non-fluoridated Kingston [5].

Fluoride in soft water is assimilated more than from hard water, and a clear correlation between percent of fluoridated water districts and heart attack incidence for the 50 U.S. States [4] is even more significant for those States in soft water regions [2].  Dr. A.L. Miller submitted data to the U.S. Congress regarding the increased incidence of cardiovascular deaths after fluoridation of Newburgh, N.Y. and Antigo, Wisconsin [5]. Electrocardiogram abnormal heart rhythms and reduced myocardial function are found in an unusually large percentage of patients having dental tooth fluorosis [6]. This is supported by recent studies indicating that patients with chronic fluorosis have detectably decreased aortic elasticity and left ventricular function [7, 8].

Although I do not support the injection of any fluoride compound into humans for any purpose, note that the study enclosed below, approved and conducted on heart disease victims for various assessment purposes, proves fluoride preferentially incorporates into damaged heart tissue in cardiac patients and into coronary and femoral arteries and aorta in these patients.  The study was conducted at the VA Health Care System in Los Angeles, CA, published in Nuclear Medicine Communications, 2011 [9]. There is no doubt that systemic fluoride incorporates directly and selectively into heart tissue and various major arteries of patients who had suffered previous heart conditions, including coronary arteries, the aorta and the leg femoral artery as well where calcium has long been known to accumulate during atherosclerosis. The incorporation of fluoride, fully expected as a toxic calcium chelator, was directly observed by Positron Emission Tomography (PET) scans after injection of radioactive fluoride as sodium fluoride.

The precise concentration in the bloodstream during the incorporation was not listed, but could be calculated by contacting the authors to determine the specific activity of the isotope employed.  Acute heart attack was obviously not induced by the injections, so the concentration was a tolerable level that did not exceed the known solubility for calcium fluoride.  At concentrations that exist in U.S. citizens in fluoridated cities, the incorporation occurs by an ion exchange mechanism, similar to that in bone where fluoride binds permanently to calcium even below the Ksp for the formed precipitate. This point is not opposed by fluoridation proponents (see attached graph from the fluoride-promoting textbook by Brun indicating bone calcium levels in fluoridated cities after lifetime accumulation).

Fluoride is a toxic calcium chelator (see original petition) and thus incorporates into tissue where calcium is enriched, including calcium-rich atherosclerotic plaque. The authors of the VA study suggested that blood fluoride is expected to increase pathologic risk in patients with cardiovascular disease and that fluoride is a component feature of atherosclerosis.  To be more accurate, fluoride itself is not a normal body component and its presence is thus an aberration. Atherosclerosis in the absence of fluoride is composed chiefly of cholesterol, calcium and fatty acids in the original fatty streak. These are normal constituents of the bloodstream and are always components of atherosclerotic plaque. Fluoride when present, not a normal body component, incorporates as an abnormal ingredient.

These charges are extremely serious. The presumption that ‘fluoridation’ is safe is based on the fact that populations with normal health, regularly drinking fluoridated water in the U.S., can live full lives to a reasonably long age. However, Dr. Albert Schatz cautioned against this mistaken assertion, since it is not the healthy with good nutrition who are noticeably most susceptible to ingestion of industrial fluorides, but rather the undernourished and infirmed who are. Specifically, the population of American citizens who suffer with atherosclerosis or cardiovascular disease are at increased risk from continuous exposure to industrial fluoride taken internally to elevate the blood fluoride level to 0.2 ppm (or higher in soft water cities). Unusual stress in heart patients is expected to be more dangerous when all organs are invested with continuous levels of the fluoride ion where it does not belong. Atherosclerosis is still considered to be the most common underlying cause of heart disease in the U.S., particularly in cases of angina pectoris substernal chest pain due to coronary artery reduced blood flow and ischemia.

Incorporation of fluoride into atherosclerotic plaque is an insidious and unnecessary abnormality that complicates atherosclerosis, the most widespread disease entity in the U.S.  Consumption of industrial fluorides from public drinking water is contraindicated in humans afflicted with either atheroscelerosis or cardiovascular disease. Much recent data, not known when the idea of ‘systemic fluoridation’ was unveiled, now prompts the elimination of industrial fluoride compounds from being intentionally injected further into public water supplies. Cardiovascular disease remains the Nation’s leading killer, and regulation and enforcement is regarded as immediately necessary.

The widespread treatment of water with industrial fluoride compounds, in a worthless attempt to decrease dental caries through internal ingestion of fluoride ion, is not the fault of the U.S. FDA.  FDA decreed in 1963 that fluoride is not a mineral nutrient and that its addition into public water supplies constitutes an uncontrolled use of a non-FDA-approved drug where dosage could not ever be regulated. Fluoridation is the fault of zealots who have routinely and completely ignored FDA statements on the matter, and the FDA is commended for not approving the ingestion of fluoride compounds and for only allowing ingestion by prescription in non-fluoridated cities. It is now time to impose regulations since currently no Federal agency assumes responsibility for the dissemination into public water supplies.

Please understand that there is no such action that can be simply called ‘fluoridation’. Fluoride cannot exist without the presence of other elements. Since 1939 when the original false correlation was made that fluoride, rather than the accompanying, responsible calcium ion, reduced teeth caries, fluoridation zealots have switched from using calcium fluoride (originally promoted as a fluoridation agent by the CDC) to sodium fluoride and then to the cheaper fluosilicic acid fluoride.  The Safe Drinking Water Act was written to prevent using public water supplies as a medium in which to disseminate any fluorides for human ingestion, but yet fluoridation promoters have sidestepped the Act by adding tacked-on regulations along the way since 1974, designed to make allowances for ill-defined ‘fluoridation’.  Fluosilicic acid supplies have now become depleted, and the next fluoride compound to be proposed to be used as source material will again be fully expected by promoters to go unnoticed and unregulated by any Federal agency.

It is simple to claim that ‘fluoridation’ is natural—simply use an agent that is known to be a natural ingredient in the earth’s crust, such as sodium, silicon, lithium, aluminum or arsenic. The first two ingredients have already been in use for ‘fluoridation’, the former for over 69 years in the U.S. Any proposed use of lithium fluoride, aluminum fluoride or arsenic fluoride for water ‘fluoridation’ could also again be argued to be ‘natural’, fully expecting complete lack of Federal agency repudiation or a ban as long as the MCL for the extra component is not exceeded.  The U.S has already entered down this slippery slope by ‘fluoridating’ water supplies with toxic industrial sodium fluoride and then with toxic hazardous waste fluosilicic acid, marketed to water districts and State public health departments as a water purifying agent with dental caries benefit as an ingestible, the substitute ingredient argued by the CDC as being ‘identical’ to natural calcium fluoride and thus deserving of the continued support and proclamation from the U.S. Surgeon General as the ‘greatest public health achievement of the 20th century’. How long this scheme continues is entirely up to the FDA, and no one else.

Sincerely,

Richard Sauerheber, Ph.D.

References:

  1. National Research Council, Report on Fluoride in Drinking Water, A Scientific Review of EPA’s Standards, Washington, D.C., 2006.
  2. Sauerheber, R., Chemical Analysis of Fluoride Poisoning from a Public Water Supply, submitted for publication in the Journal of Environmental Health, 2010.
  3. U.S. Centers for Disease Control and Prevention, Fluoride and Hydrogen Fluoride, Agency for Toxic Substances and Disease Registry, 2003.
  4. Osmunsen, B., presentation to the International Fluoride Conference, Toronto, Canada, 2007.
  5. Hardy, L., Mass harm from fluoridation, National Health Federation Bulletin, October, 1974.
  6. Xu, R. and Xu,R., Electrocardiogram analysis of patients with skeletal fluorosis, Fluoride, vol. 30, No 1, 16-18, 1997.
  7. Varol, S., et.al., Impact of Chronic Fluorosis on Left Ventricular Diastolic and Global Functions, The Science of the Total Environment, 408, No. 11,  2295-98, 2010.
  8. Varol, S., et.al., Aortic Elasticity is Impaired in Patients with Endemic Fluorosis, Biological Trace Element Research, 133, No. 2, 121-27, 2010.
  9. Yuxin, L., et.al., Association of vascular fluoride uptake with vascular calcification and coronary artery disease, Nuclear Medicine Communications: January 2012 – Volume 33 – Issue 1 – p 14–20 http://journals.lww.com/nuclearmedicinecomm/Fulltext/2012/01000/Association_of_vascular_fluoride_uptake_with.3.aspx

 

Nuclear Medicine Communications:

January 2012 – Volume 33 – Issue 1 – p 14–20

doi: 10.1097/MNM.0b013e32834c187e

Original Articles

Association of vascular fluoride uptake with vascular calcification and coronary artery disease

Li, Yuxina; Berenji, Gholam R.a; Shaba, Wisam F.a; Tafti, Bashira; Yevdayev, Ellaa; Dadparvar, Siminb

Author Information

aVA Greater Los Angeles Healthcare System, Los Angeles, California

bUniversity PA Health System, Philadelphia, Pennsylvania, USA

Correspondence to Dr Gholam R. Berenji, MD, VA Greater Los Angeles Healthcare System, Nuclear Medicine Service (115), 11301 Wilshire Blvd. Los Angeles, CA 90073, USA Tel: +1 310 268 3583; fax: +1 310 268 4916; e-mail: Gholam.Berenji@va.gov

Received June 21, 2011

Accepted August 18, 2011

Abstract

Objective: The feasibility of a fluoride positron emission tomography/computed tomography (PET/CT) scan for imaging atherosclerosis has not been well documented. The purpose of this study was to assess fluoride uptake of vascular calcification in various major arteries, including coronary arteries.

Methods: We retrospectively reviewed the imaging data and cardiovascular history of 61 patients who received whole-body sodium [18F]fluoride PET/CT studies at our institution from 2009 to 2010. Fluoride uptake and calcification in major arteries, including coronary arteries, were analyzed by both visual assessment and standardized uptake value measurement.

Results: Fluoride uptake in vascular walls was demonstrated in 361 sites of 54 (96%) patients, whereas calcification was observed in 317 sites of 49 (88%) patients. Significant correlation between fluoride uptake and calcification was observed in most of the arterial walls, except in those of the abdominal aorta. Fluoride uptake in coronary arteries was demonstrated in 28 (46%) patients and coronary calcifications were observed in 34 (56%) patients. There was significant correlation between history of cardiovascular events and presence of fluoride uptake in coronary arteries. The coronary fluoride uptake value in patients with cardiovascular events was significantly higher than in patients without cardiovascular events.

Conclusion: sodium [18F]fluoride PET/CT might be useful in the evaluation of the atherosclerotic process in major arteries, including coronary arteries. An increased fluoride uptake in coronary arteries may be associated with an increased cardiovascular risk.

Introduction

Cardiovascular disease remains the leading cause of morbidity and mortality in the world 1. The major pathophysiologic change of cardiovascular disease is atherosclerosis in critical arteries. Atherosclerosis is a slow, progressive, and cumulative process that results in atheromatous plaque formation in vascular walls and eventually leads to narrowing of the arterial lumen, occlusion, or aneurysm formation. The development of atherosclerotic plaque is characterized by subendothelial fatty material accumulation, a chronic inflammatory process, and vascular calcification 2,3. To predict and prevent any deadly cardiovascular events, extensive studies have been conducted to evaluate the risk of cardiovascular disease. Over the past decade, many cardiovascular studies focused on the calcification process in atherosclerosis 4–7.

Calcification in atherosclerosis occurs through an active process that resembles bone formation and is controlled by complex enzymatic and cellular pathways 8,9. Coronary artery calcification parallels atherosclerosis progress and is strongly and linearly correlated with the total atherosclerotic burden 10. Coronary calcification can be measured by computed tomography (CT) studies and is one of the most important predictors of future cardiovascular events. The level of coronary artery calcium can also help to reclassify asymptomatic individuals into high-risk or low-risk categories 4. Currently, sodium [18F]fluoride positron emission tomography (PET)/CT is the most sensitive imaging modality to detect active bone formation 11. Recently, Derlin et al. 12 reported the feasibility of sodium [18F]fluoride PET/CT for imaging atherosclerotic calcification in major arteries, including carotid, aorta, iliac, and femoral arteries. They also found that the mineral deposition in the carotid plaque detected by sodium [18F]fluoride PET/CT significantly correlates with atherogenic risk factors 13. Although atherosclerosis is a systemic disease, and evaluation of vascular calcification may potentially predict cardiovascular events, studies have shown that direct assessment of coronary arteries is superior to surrogate imaging for evaluating the risk of cardiovascular events 14. Some recent studies have demonstrated that evaluation of coronary arteries by PET is feasible 15–22. Most of these studies investigated fluorodeoxyglucose (FDG) uptake in coronary arteries. However, the clinical significance of [18F]fluoride uptake in coronary arteries has not been documented.

In this study, we evaluated sodium [18F]fluoride uptake in major arteries, including coronary arteries, in 61 patients. The relationship between [18F]fluoride uptake and cardiovascular history and/or multiple risk factors was also evaluated.

Materials and methods

This study has been approved by the institutional review board of the Greater Los Angeles VA Healthcare System.

Patients

We retrospectively reviewed sodium [18F]fluoride PET/CT bone studies conducted at Veterans Affairs Greater Los Angeles Healthcare System from April 2009 to June 2010. There were 58 male patients and three female patients. Detailed clinical histories and the presence of cardiovascular risk factors, such as hypertension, diabetes, hypercholesterolemia, smoking history, obesity, and history of cardiovascular events, were obtained for all patients. The clinical characteristics of the patients are summarized in Table 1.

 

Table 1
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Positron emission tomography/computed tomography protocols and imaging reconstruction

PET/CT scans were performed using a Philips Gemini TF 64-channel time-of-flight PET/CT scanner (Philips Healthcare, Andover, Massachusetts, USA) with spatial resolution of 4.5 mm at West Los Angeles VA Medical Center. Sodium [18F]fluoride was injected intravenously at a dose of 10±2 mCi (370±74 MBq). Participants were comfortably seated in a private, quiet, cozy room. Forty minutes after the injection, patients were subjected to a low-dose CT scan of the whole body without contrast at 50 mA, 120 kVp, 0.5 s/rotation, a pitch of covering 0.83 mm, and a slice thickness of 5 mm 23,24. The subsequent PET data were acquired continuously for 90 s and at 180 mm per bed position with 50% overlap between consecutive bed positions using a matrix of 140×140, followed by reconstruction corrected for attenuation using low-dose CT scans. No cardiac or respiratory gating was performed.

Imaging and statistical analyses

CT and PET images were coregistered by the Philips Extended Brilliance workstation (Philips Healthcare). CT, PET, and fused PET/CT images were evaluated visually and semiquantitatively simultaneously using the same workstation. All images were analyzed by two independent nuclear medicine physicians blinded to all patients’ clinical information. Inter-reader reproducibility was excellent and was evaluated using an intraclass correlation coefficient (0.89). Vascular calcification was identified as positive on CT images if the target was visually detectable with a greater than 130 Hounsfield units. CT-attenuated PET images were evaluated for fluoride uptake in major arteries. Background activity was based on the standardized uptake value (SUV) of the blood pool, which was calculated from the mean SUVs of three circular regions of interest (ROIs) placed in the left atrium, mid lumen of the aortic arch, and abdominal aorta at the level of the celiac trunk on axial images. The sizes of ROIs were 2 cm in diameter for the left atrium and 1 cm for the aortic arch and the abdominal aorta. Maximum SUVs (SUVmax) from target arteries were obtained by manually placing an individual circular ROI of 1 cm diameter in the target artery wall. All three orthogonal images were assessed for focal lesions in major arteries with an increased fluoride uptake. Positive fluoride uptake was identified if the target lesion was visually detectable with a greater than or equal to 1.5 target-to-background ratio in all three orthogonal image planes. For either CT or PET evaluation, the arterial territory was categorized as positive if at least one lesion was detected and agreed upon by both readers. The percentages of positive studies on both CT and PET of each arterial territory were calculated. Correlation between fluoride uptake and CT calcification was analyzed by Fisher’s exact test. Correlation of PET results and the number of cardiovascular risk factors were analyzed by the Wilcoxon rank-sum test. Significance was defined as P value of less than 0.05 in two-tailed studies.

Results

Patients’ age and reasons for sodium [18F]fluoride PET/CT imaging are summarized in Table 1. Most patients were men with a median age of 66 years (27–91 years). The majority of patients (69%) had more than one risk factor for coronary artery disease.

Arterial sodium [18F]fluoride uptake and calcification

Arterial wall sodium [18F]fluoride uptake and calcification were evaluated in major arteries, including carotid arteries, the thoracic ascending (including aortic arch) aorta, the thoracic descending aorta, the abdominal aorta, femoral arteries, and major branches of coronary arteries. Iliac arteries were not evaluated because of frequently observed urinary and occasional bowel uptake in the pelvis, which interferes with the accurate assessment of iliac vessels. For coronary arteries, four major branches were evaluated. An example of fluoride uptake in femoral arteries is shown in Fig. 1. Orthogonal views of fluoride uptake in the aorta and coronary arteries are shown in Figs 2 and 3.

Fig. 1
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Fig. 2
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Fig. 3
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Both fluoride uptake and calcification were common in major arteries as summarized in Table 2. In general, fluoride uptakes in vascular walls were observed in 361 vascular territories of 59 (97%) patients, and calcifications were observed in 317 vascular territories of 49 (88%) patients. Only two patients did not demonstrate fluoride uptake in any of the vasculatures (one patient aged 27 and one aged 61). In thoracic aortas, the abdominal aorta, and femoral arteries, fluoride uptake was observed more frequently compared with calcification. In contrast, calcification was more common than fluoride uptake in carotid and coronary arteries (Table 2). Except for the abdominal aorta, fluoride uptake and calcification were significantly correlated in the same vascular territories, as evaluated by Fisher’s exact test. It should be noted that the fluoride uptake and calcification were not necessarily overlapped in the exact same anatomic locations. At calcification sites that did not demonstrate prominent overlapping fluoride uptake, fluoride uptake was frequently observed in the adjacent area within the same arterial territories (Fig. 2).

 

Table 2
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Relationship between coronary fluoride uptake and cardiovascular risk factors

The coronary arteries were also investigated for fluoride uptake. Four major branches of coronary arteries, including left main artery (LMA), left anterior descending (LAD), left circumflex (LCA), and right coronary arteriy (RCA) were evaluated. Fluoride uptake was more frequently observed in the LAD and LCAs. A similar pattern was also identified in coronary artery calcification. In each individual coronary branch, calcification was more frequently observed than fluoride uptake (Table 2). Among 10 patients who had significant three-vessel coronary calcifications, 80% demonstrated fluoride uptake in at least one coronary branch (data not shown).

Cardiovascular risk factors including hypertension, obesity, diabetes, hypercholesterolemia, smoking history, and history of coronary artery disease were reviewed in all patients (Table 3). The majority of the patients (69%) had more than one cardiovascular risk factor; however, neither the individual cardiovascular risk factor nor the number of risk factors was significantly correlated with coronary fluoride uptake (Table 3). Nine patients had a history of cardiovascular events. Among them, eight demonstrated identifiable coronary fluoride uptake. There was significant correlation between coronary calcification and fluoride uptake in this group evaluated by Fisher’s exact test (Table 3). All nine patients also demonstrated coronary calcification on CT images. We also compared the SUVmax in coronary arteries between patients with and without a history of cardiovascular events. The average coronary SUVmax in patients with a history of cardiovascular events was 1.70, significantly higher than 1.39 for patients without a history of cardiovascular events (P=0.029, two-tailed Student’s t-test). No correlation was observed between cardiovascular risk factors and fluoride uptake in other vascular territories (noncoronary).

 

Table 3
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Discussion

Vascular calcification, in particular coronary calcification, has been shown to predict vascular events 25–27. Recent utilization of multidetector CT has made the assessment of coronary calcium feasible and reproducible 7,28. However, CT can only evaluate structural change, which usually represents later stages of the disease’s process. Given the assumption that fluoride uptake represents dynamic atherosclerotic calcification, we would expect that fluoride uptake occurs at the stage before the formation of detectable calcium deposition. Consistent with this theory, Derlin et al. 12 reported that only 12% of the calcification sites demonstrated prominent overlapping fluoride uptake, whereas 12% of fluoride-positive lesions did not show concordant calcification. In our study, fluoride uptake and CT calcification are significantly correlated in the same arterial territories, except in the abdominal aorta. This is because of the extremely high positive rate (97%, only one patient demonstrated negative uptake) for fluoride uptake in the abdominal aorta. Fluoride uptake either overlaps with calcification or locates adjacent to the detectable calcium deposits, suggesting that fluoride uptake and detectable calcification represent different stages of the atherosclerotic process.

In large arteries, such as the thoracic aorta, abdominal aorta, and femoral arteries, fluoride uptake is more commonly observed than calcification. This finding is different from results published by Derlin et al. 12, which demonstrated that fluoride uptake is less frequently observed than calcification in all major arteries. The discrepancy may be due to different PET/CT scanners. In our study, we used a time-of-flight PET/CT scanner with better spatial resolution (4.5 mm vs. 8 mm) and higher sensitivity. In addition, differences in patient populations may also contribute to the discrepancy. Most of our patients were older male veterans with multiple cardiovascular risk factors. Consistent with this, our data demonstrated notably higher incidents of calcification compared with the data published by Derlin et al. 12. Recently, they also reported that fluoride uptake in carotid arteries significantly correlated with cardiovascular risk factors. We found that 43 (right) and 48% (left) of patients have carotid calcifications, whereas 34 (right) and 38% (left) of patients have fluoride uptake, compared with 32 (right) and 37% (left) with calcification and 25 (right) and 28% (left) with fluoride uptake according to the results from Derlin et al. 13. However, we did not observe any correlation between carotid fluoride uptake and cardiovascular risk factors, probably because of the limited number of patients in our study.

In contrast to the results of the aorta and femoral arteries, fluoride uptake was less commonly observed than calcification in coronary arteries. This phenomenon could be due to the following reasons: (a) the limited spatial resolution of PET reduces the sensitivity to detect fluoride uptake in smaller arteries; (b) the combination of cardiac and respiratory motions further reduces the sensitivity of PET in the evaluation of coronary arteries; (c) the proximal coronary arteries are surrounded by vascular structures that are highly susceptible to calcification. These include aorta, pulmonary artery, and heart valves. All these structures may affect the interpretation of fluoride uptake in coronary arteries; and (d) the partial volume effect on the small size of the ROIs is also a possible reason.

Coronary motion is greatest in the RCA, followed by circumflex coronary artery, LAD, and LMA in descending order 29. Our study demonstrated that fluoride uptake was more frequently observed in LAD and circumflex coronary artery than in the RCA and LMA. Motion artifact reduces the sensitivity to detect fluoride uptake in the RCA. The short length of LMA and its short distance to the aorta, which frequently demonstrates fluoride uptake, may attribute to the low frequency of fluoride uptake in the LMA. Despite the feasibility of fluoride PET evaluation of coronary calcification, coronary imaging with fluoride PET/CT remains challenging because of small artery size, motion artifact, and interference of surrounding vasculature calcifications. All of these factors will potentially cause either false-negative or false-positive results. The recent development of cardiac–respiratory gating technology in PET scans may increase the accuracy of coronary imaging 30–32. In addition to the technical difficulties in evaluating coronary arteries, the limited number of patients and the unvarying nature of the patient population in this study may be skewed and may not apply to the general population.

We found that fluoride uptake in coronary arteries is significantly correlated with a patient’s history of cardiovascular events, and the uptake value in patients with cardiovascular events was significantly higher than that in patients without cardiovascular events. These results further support the fact that higher fluoride uptake in coronary arteries indicates increased cardiovascular risk. Recently, several studies have demonstrated the feasibility of FDG-PET/CT in detecting plaque inflammation in coronary arteries 15–22. Nevertheless, fluoride PET/CT detects active mineral deposition, which represents the distinct pathophysiologic process of atherosclerosis. Derlin et al. 33 reported that uptake of FDG and sodium fluoride in vessel wall alterations was rarely coincident, supporting the suggestion that these two studies evaluate different functional and morphologic changes of the atherosclerotic process. The FDG uptake and fluoride uptake of atherosclerotic plaques could have complementary roles in evaluating the cardiovascular risk of patients. The combination of sodium [18F]fluoride PET and CT is a promising imaging modality that provides both metabolic and anatomic information in evaluating vascular calcification. However, large-scale studies are needed to evaluate the clinical significance of fluoride PET/CT for imaging atherosclerosis.

Conclusion

Our study demonstrates that vascular calcification and fluoride uptake are significantly correlated in the same arterial territory, although not necessarily overlapping in the same anatomic locations. An increased fluoride uptake in coronary arteries may be associated with an increased cardiovascular risk. Combined anatomic and metabolic imaging with sodium [18F]fluoride PET/CT offers a promising, noninvasive method to evaluate atherosclerosis.

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27. Raggi P, Cooil B, Callister TQ. Use of electron beam tomography data to develop models for prediction of hard coronary events. Am Heart J. 2001;141:375–382

28. McCollough CH, Ulzheimer S, Halliburton SS, Shanneik K, White RD, Kalender WA. Coronary artery calcium: a multi-institutional, multimanufacturer international standard for quantification at cardiac CT. Radiology. 2007;243:527–538

29. Lu B, Mao SS, Zhuang N, Bakhsheshi H, Yamamoto H, Takasu J, et al. Coronary artery motion during the cardiac cycle and optimal ECG triggering for coronary artery imaging. Invest Radiol. 2001;36:250–256

30. Martinez-Moller A, Zikic D, Botnar RM, Bundschuh RA, Howe W, Ziegler SI, et al. Dual cardiac-respiratory gated PET: implementation and results from a feasibility study. Eur J Nucl Med Mol Imaging. 2007;34:1447–1454

31. Buther F, Dawood M, Stegger L, Wubbeling F, Schafers M, Schober O, et al. List mode-driven cardiac and respiratory gating in PET. J Nucl Med. 2009;50:674–681

32. Teras M, Kokki T, Durand-Schaefer N, Noponen T, Pietila M, Kiss J, et al. Dual-gated cardiac PET-clinical feasibility study. Eur J Nucl Med Mol Imaging. 2010;37:505–516

33. Derlin T, Toth Z, Papp L, Wisotzki C, Apostolova I, Habermann CR, et al. Correlation of inflammation assessed by 18 F-FDG PET, active mineral deposition assessed by 18 F-Fluoride PET, and vascular calcification in atherosclerotic plaque: a dual-tracer PET/CT study. J Nucl Med. 2011;52:1020–1027

***

 

II.Fluosilicic Acid Industrial Fluoride Removed from Fluoridated Selmer, Tennessee.

The letter below was sent to San Diego Mayor Sanders, in an attempt to appease San Diego citizens, and myself, by asking the Mayor a favor that is not unreasonable. David Robinson, the Mayor of Selmer, Tennessee asked a few questions of the fluosilicic acid suppliers for his city and found the supplier could not provide such answers, and instead ceased to provide any further the specific fluosilicic acid formulation that had been used in Selmer for years, and then removed all fluoridation equipment and chemicals from Selmer (see Robinson letter attached). Mayor Robinson has agreed to send the correspondence he has to Mayor Sanders, if it is requested. Here is an attempt to obtain that information to have on file for the city of San Diego for reference because of use by San Diego of the same fluoridation materials used in Selmer.

Dear Mayor Sanders,

I am writing to ask a simple specific favor of you.  You are fully aware of my feelings on this, but this request is not related to either the support of, nor the opposition to, water fluoridation and is not dependent on scientific data.  David Robinson, the Mayor of Selmer, Tennessee wrote to me that he will provide information he obtained that resolved this issue in Selmer, that is similar to that in San Diego.  Selmer City officials in the fully fluoridated state of Tennessee found itself in a position similar to here in San Diego, where citizens opposed a measure that is nevertheless required, as here by the CA State fluoridation bill.  It is a great story and I’m certain you will be happy that you contacted him, in particular because in so doing you will have the latest information that will fulfill your obligations of due diligence for duty of care for citizens here.

Thank you for your consideration of this request, for the benefit of our city.

Robinson is a good and effective mayor and he wrote that he will be more than happy to forward the brief correspondence he has if you ask. His contact information he sent me is:

David Robinson

Mayor, Town of Selmer

City Hall  731-645-3241

Cell         731-610-7016

Fax         731-646-1462

 

***

III. Correspondence with the Office of Drinking Water, U.S. Environmental Protection Agency, Region 9, San Francisco.

The FDA 2010 response to the 2007 petition stated that “artificial fluoride compounds used to fluoridate public drinking water…is regulated by the U.S. Environmental Protection Agency (EPA) under the Safe Drinking Water Act of 1974 (SDWA).” To clarify for you the actual official belief held by the EPA, enclosed please find letters of communication with Jill Korte, U.S.  EPA, Region 9, San Francisco, CA, Office of Drinking Water.

The following letters were recently exchanged with U.S. EPA Region 9.  In summary, the EPA mistakenly proposes that fluoride is a contaminant and as long as the level is not in excess of the MCL of 2 ppm, EPA does not take action. In the letter it was admitted that no Federal requirement is allowed for agents added into water to treat people, but that EPA is not concerned with this because the EPA itself does not recommend or support the injections. Intentional injections, although in violation of the SDWA, will not be enforced until the level exceeds the allowed level for fluoride pollution at 2 ppm. In other words, EPA will do no regulating of the procedures by which fluoride compounds are titrated into water, and EPA basically views the MCL as an invitation to ‘fill ‘er up’ with a substance that is not allowed by the SDWA.

Notice my response to the EPA indicates that we all need to follow the SDWA and prohibit adding any purported medicaments or other agents into water supplies other than to sterilize the water, and that adding a fluoride compound violates the Act. No industry or private agency or citizen is allowed to add any contaminant or other substance into water simply because the total concentration after dilution is kept below the MCL that EPA has decided to allow for a pollutant. The EPA is using the MCL as though it is a value assigned for an ingestible substance approved with proper regulations required by the Food Drug & Cosmetic Act. Understand though that only proper prospective controlled human clinical trials data may be used to arrive at a daily dose for any purported ingestible compound to be taken internally, as required by the FD&CA.

I apologize for the unnecessary side topic of arsenic being mistakenly typed in a wrong column on a Water District report, rather than being an actual water error, as you will see in the exchange.

      Richard D. Sauerheber, Ph.D.
Palomar Community College
1140 W. Mission Rd., San Marcos, CA 92069
E-mail: richsauerheb@hotmail.com   Phone: 760-402-1173

 

U.S. Environmental Protection Agency
Region 9, San Francisco, CA
Drinking Water Office

Dear Jill Korte,
The U.S. EPA of course is not itself directly violating the U.S. Safe Drinking Water Act.  I realize that the EPA is not adding fluosilicic acid and is not recommending its addition either.  But what you fail to see is that the State of California is in violation of the SDWA because indeed the State, under the direction of Federal dental officials at the Oral Health Division of the Centers for Disease Control by their request, is indeed adding an agent to treat humans through the public water supply, in violation of the Act.

You have claimed in your letter that the EPA allows the INTENTIONAL injection of chemical substances to treat humans through drinking water as long as the final dilution level remains below the EPA MCL for fluoride.  This is absurd. Understand that the 2 ppm MCL you mention is the allowed level for fluoride as an accidental or naturally-present contaminant.  It is NOT an invitation to ‘fill ‘er up’ with fluoride on purpose, as long as it remains below 2 ppm when you are done.  Intentionally adding a contaminant violates the SDWA just as much as intentionally adding a substance to treat humans violates the Act.  Remaining below 2 ppm does not give one the right to willfully place any substance into public water supplies.

If you as a public servant feel this way and interpret the original Congressionally-approved statutes of the SDWA that way, then please consider this:

The next time someone dumps barrels of pure arsenic into a public water supply, you have no right whatsoever to arrest him or prohibit his actions, as long as he carefully titrates it in so that the final level does not exceed the MCL for these materials that is allowed by the EPA.

Do you understand how absurd your thinking is? EPA Region 9 is a basically useless entity in helping spare the people of this country and our State from the intentional treatment of the human blood supply with industrial fluoride through drinking water. Why do you support such nonsense? EPA scientists are currently in litigation over this very matter (Connett, et.al., The Case Against Fluoride, 2010). EPA has every right to order the halt of intentionally-injected contaminants into public water supplies because the EPA is entrained to follow and enforce the SDWA as much as public citizens and anyone else in this country is obligated to honor.  Indeed, as you may know, EPA scientists have published that we must stop using our Nation’s water supplies as a vehicle to dispose of toxic hazardous waste fluosilicic acid.  How long does the public need to wait for help from EPA administrators?

Finally, as a chemist who is fully aware of methodology required to eliminate fluoride contamination from drinking water, please understand that the CA Department of Public Health routinely ‘certifies’ reverse osmosis units as ‘reducing fluoride by 90%.’ This is a deceptive and evil practice. In detailed interviews, chemists who perform the tests admitted that this type of reduction cannot be obtained when starting with fluoride concentrations present by intent in public water supplies.  90% reduction is only obtained when starting with fluoride levels in excess of the Ksp solubility for calcium fluoride. In other words, at 8-9 ppm fluoride where calcium fluoride precipitates as particles, of course RO easily removes them. The same instrument however is incapable of but a mere 30% or less reduction when the input water is 1-2 ppm fluoride.  Fluoride removal from treated public water under conditions of current use is an expensive and non-trivial issue. Engineers have recently developed special ultra tiny pore size membranes that under high pressure can separate water from fluoride by forcing the oblong water molecule through a pore that tiny fluoride ion cannot enter, but only recently have these become available retail. Also animal bone char (Brimac), only available from facilities in Scotland, is capable of eliminating fluoride by ion exchange much like live bone can, so one’s own bones do not incorporate it. These are the only two methods that work for drinking water, and only the latter method is usable for whole house use for those who cannot shower with fluosilicic acid water due to fluoride allergy. RO wastes far too much water for every gallon produced. And whole house bone char is very expensive to maintain, particularly with Brimac shortages that already exist.

It would greatly benefit you if you could please examine the above Connett text and also the National Research Council Report on Fluoride in Drinking Water, A Scientific Review of EPA’s Standards, Washington, D.C., 2006 that the EPA commissioned to investigate this specific issue. The NRC concluded without reservation that the current allowed EPA MCL for fluoride is not protective of human health. This is consistent with the current CDC-documented epidemic of tooth fluorosis we now have in 41% of American children aged 12-15 as of 2001 that prompted the U.S. Health and Human Services to request water levels not exceed 0.7 ppm as an interim measure until the issue of ‘water fluoridation’ is resolved. FDA has never approved ingestion of fluoride compounds from public water supplies and has never allowed sale of fluoride compounds to be taken internally without a prescription. The petition to ban fluosilicic acid injections into water supplies in the U.S., accepted for review by the FDA in 2007 (FDA-2007-P-0346), is still pending.

We again ask the EPA to enforce the SDWA in the meantime, in particular for us here in Carlsbad, CA. The National Sanitation Foundation private organization Standard 60 ‘certification’ mark is devoid of controlled human clinical trials data to back it up, as the FDA recognizes.  EPA has a long way to go to catch up on this National abuse of a substance that continues without regulation by any Federal office that agrees to accept liability or responsibility for the treatments.

You might also want to contact Mayor David Robinson of Selmer, Tennessee who will provide letters indicating that fluosilicic acid suppliers do not have any data demonstrating caries reduction in those who consume their product and have no evidence of safety for long-term consumption, particularly in the infirmed.  An EPA MCL is not an allowance to ingest a substance intentionally for its drug-like effects.  Food Drug and Cosmetic Act regulations must be satisfied for any such substance used as an ingestible. If you seek, you will find that the FDA ruled fluoride in water is an uncontrolled use of an un-approved drug and is not a mineral nutrient.

The FDA is not in an as easy a position as is the EPA to ban the injections or to prohibit them for selected locations in honor of the SDWA. And this is why we are asking you to act on this request instead of dismissing it on paper.

 

To: richsauerheb@hotmail.com

CC: Jones.Joel@epamail.epa.gov; Pringle.Everett@epamail.epa.gov; Sylls.Gene@epamail.epa.gov

Subject: Fw: (SDWA – FY12-91141-3715-CV) Referred to Region – California

From: Korte.Jill@epamail.epa.gov

Date: Wed, 8 Feb 2012 09:22:55 -0800

Dear Dr. Sauerheber,

Thank you for your e-mails of 1/10/2012 regarding the Metropolitan Water’s (MWD) treated drinking water supply that is provided to Carlsbad Water District.  You asked that EPA request that Carlsbad water not be treated with fluoridation materials by MWD due to your health concerns about fluoride and potential impurities in hydrofluosilicic acid, such as arsenic.  The drinking water supplied by Carlsbad Water District is in compliance with the federal and state standards for both fluoride and arsenic.  Furthermore, the State of California meets its obligations under the Safe Drinking Water Act for the delegation of primary enforcement authority for the public water supply supervision program with respect to the fluoride standard.  The U.S. EPA cannot request that MWD stop fluoridation of its water supply.

The Safe Drinking Water Act (SDWA), 42 USC §300g-1(b)(11), does prohibit the federal government from adopting any national primary drinking water regulations that “require the addition of any substance for preventive health care purposes unrelated to contamination of drinking water.”  The U.S. EPA has not adopted any national regulations requiring the addition of fluoride or any other substance for preventive health care.

The SDWA, 42 USC §300g-2(a)(1), requires states such as California that have been granted primacy enforcement responsibility for public water systems to “adopt drinking water regulations that are no less stringent than the national primary drinking water regulations.”  With respect to fluoride, the U.S. EPA has adopted a health-based, enforceable, primary standard of 4.0 mg/l and a secondary standard of 2.0 mg/l that is based on the cosmetic effects of dental fluorosis.  Under federal regulations, public water systems with fluoride levels greater than 2.0 mg/l but less than 4.0 mg/l are subject to specific public notification requirements, but are not required to treat to levels 2.0 mg/l or less.  California’s enforceable, primary standard for fluoride is 2.0 mg/l, making the state regulation more stringent than the federal regulation.  Although California does require its larger public water systems to fluoridate, they are assigned an optimal fluoride level and must operate within a control range, the upper limit of which is less than the more stringent, state enforceable maximum contaminant level (MCL) of 2.0 mg/l.

Metropolitan Water District’s Skinner Water Treatment Plant provides water to Carlsbad Water District and consistently produces water that is well below the MCLs for both the state and federal fluoride and arsenic MCLs. Arsenic is not detected in the MWD supply from the Skinner Treatment Plant.  In addition, treated water provided to Carlsbad Water District by the San Diego County Water Authority also meets both federal and state standards for fluoride and arsenic.

Any questions you have on fluoridation or home treatment units for fluoride removal should be directed to the California Department of Public Health in Sacramento at (916) 449-5600.

Thank you for your interest in this topic.

Sincerely,

Jill Korte, P.E.

Environmental Engineer

CA PWSS Project Officer

U.S. EPA Region 9

Drinking Water Office

75 Hawthorne St. (WTR-6)

San Francisco, CA 94105

(415) 972-3562  (415) 947-3549 (fax)

01/10/2012
SUBJECT:    FWD: (SDWA – FY12-91141-3715-CV) Referred to Region – CaliforniaFROM:    sylls.gene@epa.govTO:    jones.joel@epa.gov

CC:

See complaint #91144. The following tip is from the National Tips Database. This information is being provided to you for whatever action you deem appropriate. Please follow up or notify the appropriate agency.

1/4/2012 8:46 PM
HQ LEAD NUMBER:    FY12-91141-3715-CV
SUBJECT:    Referred to Region – California
FROM:    richsauerheb@hotmail.com
TO:
Name:  Dr. Richard Sauerheber
Address:  1826 Redwing. St.
City:  San Marcos
State:  California
Zip:  92078
Phone:  760-744-2547
Alleged Violator’s Name:  Carlsbad Water District
Alleged Violator’s Address:  5950 El Camino Real
Alleged Violator’s City:  Carlsbad
Alleged Violator’s State:  California
Alleged Violator’s Zip:  92008
Tip or Complaint:I here raise a formal complaint against the Carlsbad Water District, San Diego County for its use of water with high arsenic levels, and for not reporting this clearly. A value of 120 ppb arsenic detected was listed on their water quality report 2011 with an average of 1.9 ppb. As you know, the EPA allowed MCL for arsenic since Jan., 2011 has been 10 – 50 ppb. The CA State MCL is 10 ppb and the State Public Health Goal is zero. A small amount of arsenic is diluted into water from added fluosilicic acid crude preparations that use the excuse of fighting cavities with the fluoride contained in it. Again, the As PHG is zero. Further, it is a violation of the Safe Drinking Water Act for any State to be less restrictive than its clause that prohibits any National requirement for any substance added into water other than to sanitize the water. This makes it illegal to add arsenic, fluoride, or any substance other than to kill bacteria, into water and yet the practice of adding both has now spread even here to Southern CA recently against the voting willl of the public. These were the typed data in the Carlsbad Water Quality Report, 2011. Arsenic: CA MCL 10 ppb; PHG .004 Sample 1.9 Range ND – 120 I was told by an employee of CWD that the 120 number was not a reading, but an ‘allowed range’. But again the Fed and State allowed ranges do not include a number as high as 120 ppb. I told him that and he said he wasn’t sure and that I need to talk with the supervisor who is not available. The 120 number was printed in the report in the column in which measurements were reported, not in the column which lists the allowed MCL’s, as shown above.If you could look into this we would appreciate it here in Carlsbad. We have had a terrible history with elementary school children perishing with cancers of various types and we are aware of the problem with schoolhouses being built on farms (as here) where arsenic pesticides had been used and that allowed arsenic emissions are detected from the Carlsbad emission stacks from a utility. The last thing Carlsbad children need is an extra dose of arsenic from their local water supply and yet that is what they are getting, from fluosilicic acid diluted waste and obviously additional unknown sources responsible for these readings. Carlsbad should be placed on a moratorium for the addition of crude hazardous diluted fluosilicic acid waste, out of sheer courtesy to the parents of these children as well as for the safety of the children themselves.

We in So CA have had enough of fluosilicic acid waste that actually adds, for every 30 tons of added materials, 10 tons of sodium in fresh water where it does not belong, 10 tons of fluoride unwanted by the citizens, and 10 tons of silicic acid, all labeled as ‘water fluoridation.’ When does drugging the people of a city end, and who has the right to alter the bone density of citizens with fluoride that we now know crosses the blood brain barrier and injects arsenic when we are trying to remove it under our specific problematic circumstances?

Violation Still Occurring? Yes
State DEP/DEQ/DEM Notified? No

01/10/2012

SUBJECT:    FWD: (SDWA – FY12-91144-3715-CV) Referred to Region – CaliforniaFROM:    sylls.gene@epa.govTO:    jones.joel@epa.gov

CC:

See complaint #91141. The following tip is from the National Tips Database. This information is being provided to you for whatever action you deem appropriate. Please follow up or notify the appropriate agency.

1/4/2012 11:10 PM
HQ LEAD NUMBER:    FY12-91144-3715-CV
SUBJECT:    Referred to Region – California
FROM:    richsauerheb@hotmail.com
TO:
Name:  Dr. Richard Sauerheber
Address:  1826 Redwing St.
City:  San Marcos
State:  California
Zip:  92078
Phone:  760-744-2547
Alleged Violator’s Name:  Metropolitan Water District
Alleged Violator’s Address:  Alameda St.
Alleged Violator’s City:  Los Angeles
Alleged Violator’s State:  California
Alleged Violator’s Zip:  90054
Tip or Complaint:I earlier submitted a complaint against Carlsbad Water District, CA on behalf of children in that city. Upon reading the Vallecitos Water Report that shares the same water source, it became clear that the Carlsbad Water Quality Report made a simple clerical error and typed in a value of 120 ppb for arsenic that was actually that for barium, which is an acceptable number. The remaining part of the original complaint then is directed to Metropolitan Water, Los Angeles, because Carlsbad does not inject the fluosilicic acid materials, but rather MWD does. MWD is unaware of the arsenic issue in Carlsbad, where arsenic in schoolyard soils and from the city power plant stack parents believe is causing the high incidence of childhood cancers here. The type and class IA human carcinogen arsenic is present in small amounts in the fluosilicic acid injected for its fluoride by MWD and we ask the EPA to request that Carlsbad water not be treated with fluoridation materials by MWD, particularly inasmuch as fluoride in blood at 0.2 ppm inhibits DNA repair enzymes involved in cancer cell removal (Yiamouyiannis, Fluoride, The Aging Factor, 1985; National Research Council, Report on Fluoride in Drinking Water, 2006; Connett, The Case Against Fluoride, 2010) and because Carlsbad Water has arsenic and lead at levels approaching their respective MCL’s both at the same time.Fluosilicic acid waste injections are requested by Federal dentists at the CDC, which is prohibited by the Safe Drinking Water Act since no National requirement may be made for any substance added into water other than to sanitize the water, and States can be no less restrictive. Ingested fluoride is not FDA approved, and States cannot require consumption by citizens of a substance that is not FDA approved. Carlsbad citizens are being disserved by EPA allowance of fluosilicic acid hazardous waste injections into city water supplies that violates the SDWA. The National Sanitation Foundation is a private agency that ‘certifies’ the injection materials without having data demonstrating it is effective at caries reduction or that it causes no harm to anyone upon long term consumption. The chemical supplier Lucier Chemicals and Brenntag Chemicals likewise have no such data demonstrating safety or effectiveness of the materials they sell and deliver to MWD and to San Diego (personal communication, Brenntag CEO, water chemicals division).

Carlsbad water also contains injected aluminum at 0.05 ppm which forms complexes with fluoride in stomach acid. Fluoride crosses the blood brain barrier, affects calcium homeostasis and induces bone cell division as a result. These children with high incidence of various lethal cancers in Carlsbad are being subject to unnecessary risk with fluoridation waste materials that is inconsistent with current conditions here. Thank you for your attention.

Violation Still Occurring? Yes
State DEP/DEQ/DEM Notified? Yes

 

 

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