Despite the fact that Sodium Fluoride “is a persistent, non-degradable poison that moves through the environment and accumulates in the soil and organisms” (Waste Not #461) the USDA is allowing for its use in the new National Organic Standards which are nearing completion. We need to act now to ensure that organic food production does not contribute to our already excessive exposure to fluoride. The USDA is accepting comments up until June 12. So please add your voice to this matter and remind the USDA that
*Section 6508 (c)1 of the New Organic Standards says that producers shall not use “poisons such as arsenic and lead salts that have long-term effects and persist in the evironment.” Fluoride is in this category.
*Chronic ingestion of fluoride has been associated with damage to kidneys,teeth, and bone (5); increased hip fractures in the elderly (6-13); bone spurs (14); stress fractures (15); and osteosarcoma (bone cancer) in young males (16-18). Fluoride collects in the aorta, skin, skeleton, and cataracts. It causes calcifications in joints, soft tissues, and in and around teeth (19), and disturbs the formation of collagen (20).
*Fluoride concentrates in the pineal gland with a decrease in production of melatonin, accompanied by early puberty in gerbils (21,22) and perhaps in young girls (23).
*Fluoride passes the placenta from the mother’s blood to the developing fetus (24-26) and can interfere with calcification of bones and formation of teeth (27,28).
*Two recent animal studies reported that fluoride accumulates in the brain (29,30). Fluoride enables aluminum to enter the brain; aluminum appears to associate with the protein tangles seen in Alzheimer’s disease (29). Other studies suggest fluoride exposure may have adverse impacts on the developing brain (31).
(The above are excerpts taken from Waste Not #461, which was written by Ellen Connett and Jackie Jacobson, and which is presented in full at the website address given above)
References:
6. Agency for Toxic Substances and Disease Registry (ATSDR). 1993. Toxicological profile for fluorides, hydrogen fluoride, and fluorine (F). U.S. Department of Health & Human Services, Public Health Service. p 56-57.
7. Danielson C, et al. 1992. Hip fractures and fluoridation in the Utah’s elderly population. JAMA, 268, 746-748.
8. Jacobsen SJ, et al. 1992. The association between water fluoridation and hip fracture among white women and men aged 65 years and older. Annals of Epidemiology, 2, 617-626.
9. Jacobsen SJ, et al. 1990. Regional variation in the incidence of hip fracture. US white women aged 65 years and older. JAMA, 264, 500-502.
10. Cooper C, et al. 1991. Water fluoridation and hip fracture (letter). JAMA, 266, 513-514.
11. Jacqmin-Gadda H, et al. 1995. Fluorine concentration in drinking water and fractures in the elderly (letter). JAMA, 273, 775-776.
12. Sowers MR, et al. 1991. A prospective study of bone mineral content and fracture in communities with differential fluoride exposure. American Journal of Epidemiology, 133, 6649-660.
13. Cooper C, Wickham CAC, Barker DJR, Jacobson SJ. 1991. Water fluoridation and hip fracture [letter]. JAMA, 266 513-514.
14. Waldbott GL, Burgstahler, AW, McKinney, HL. 1978. Fluoridation: the great dilemma. p.199, Fig. 12-4; p 200, Fig 12-5.
15. Schlesinger ER, et al. 1956. Newburgh-Kingston Caries-Fluorine Study XIII. Pediatric Findings After ten Years. JADA, 52.
16. Waldbott et al. 1978. p 225.
17. Cohn PD. 1992. An epidemiologic report on drinking water and fluoridation. New Jersey Department of Health, Trenton, NJ.
18. National Toxicology Program. 1991. Toxicology and carcinogenesis studies of sodium fluoride in F344/N rats and B6C3F1 mice. NTP Report No. 393.
19. Waldbott et al. 1978. p 151-153; p 166; p 99, 195; p 151-153; p 183-184.
20. Yiamouyiannis J. 1993. Fluoride the aging factor. Health Action Press. Chapter 4 et al.
21. Luke J. 1994. Effects of fluoride on the physiology of the pineal gland. Caries Research, 28, 204.
22. Luke J. 1998. Effects of fluoride on the physiology of the pineal gland in the mongolian gerbil meriones unguiculatus. Paper presented at the 22nd Conference of the International Society for Fluoride Research, Bellingham, Washington. August 24-27.
23. Schlesinger ER, et al. 1956. (Note: Girls were found to have reached menstruation five months earlier, on average, in fluoridated Newburgh compared to girls in non-fluoridated Kingston.)
24. ATSDR, 1993. p 6, 83-84.
25. Cassarett and Dooull. 1975. Toxicology. p 717.
26. Smith and Smith. 1935. JADA, 22: 814-817.
27. Crops in Peace and War. USDA Yearbook 1950-51. p. 722
28.. Fleming HS and Greenfield. 1954. Changes in the teeth and jaws of neonatal webter mice after administration of NaF and CaF2 to the female parent during gestation. J Dental Res, 33:780-788.
29. Varner JA, et al. 1998. Chronic administration of aluminum-fluoride and sodium-fluoride to rats in drinking water: alterations in neuronal and cerebrovascular integrity. Brain Research, 784, 284-298.
30. Mullenix P, et al. 1995. Neurotoxicity of sodium fluoride in rats. Neurotoxicology and Teratology, 17, 169-177.
31. Schettler T, Stein J, Reich F, Valenti M, Wallinga D. May 2000. In Harm’s Way: Toxic Threats to Child Development. Greater Boston Physicians for Social Responsibility. p 90-92. (www.igc.org/psr/ )
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