May 24, 2000

Action Request: Send Comments to USDA on Proposed National Organic Standards requesting that they prohibit sodium fluoride as an allowed substance in the production of organic food

Submit Comments to USDA
Comments due by: June 12, 2000

In the proposed National Organic Standards Rule (the Rule), the USDA states its intention to allow the use of EPA's List 4 Inerts as Allowed Substances for the production and handling of organic food... unless specifically prohibited.

The List 4 Inerts includes sodium fluoride (NaF), but NaF should be specifically prohibited for use in the Rule for a number of reasons.

* Because fluoride is "pesticidally active" and "of toxicological concern", it never should have been on EPA's List 4 Inerts (nonactive ingredients).

* Section 6508 (c)1 of the Rule says producers shall not use "natural poisons such as arsenic or lead salts that have long-term effects and persist in the environment." Fluoride is in this category.

* The broad spectrum of fluoride's toxic abilities makes it especially inappropriate for use in sustainable, organic agriculture.

* Fluoride is a persistent, non-degradable poison that moves through the environment and accumulates in the soil and organisms. It damages crops, livestock, wildlife, and human health.

The National Organic Standards (NOS) rule allows the use of most of the substances on EPA's List 4 of "inert" substances. Formerly "inerts" included anything in a pesticide formulation not claimed as an "active ingredient" for killing a target organism, even if these "other" substances were also toxic and pesticidal. Some, especially cumulative poisons, have no place in organic activities and sustainable agriculture.

According to USDA (1) "compounds that contain fluorine" have been used as pesticides since 1890 on a wide variety of insects and crops. They rank with lead and arsenical poisons in toxicity. NaF was often used as a roach powder and rat poison and against chicken and animal lice. "It causes serious damage on plants," said USDA. Today NaF is used in insecticides, as a preservative for wood and glue, and to disinfect equipment in breweries and distilleries (2).

A pharmacology laboratory was established in USDA in 1931 (3). Its first assignment was to determine the chronic toxicity of inorganic fluorine compounds used as pesticides (sodium fluoride, sodium fluosilicate, barium fluosilicate, and sodium aluminum fluoride [cryolite]) in order to set tolerances. All of these salts were sufficiently soluble and absorbable to cause mottling of teeth in white rats. The fluoride ion also delayed calcification of leg bones in young rats.

Fluorides can concentrate in plants and accumulate in soils, especially through the application of untreated phosphate rock. This fertilizer contains 3-5% fluoride. In 1938 (4) USDA sagely warned farmers to minimize the "fluorine applied with commercial fertilizers. The use of fluorine compounds as insecticides is growing, and in years to come the quantity of fluorine added to soils through this source may be considerable."

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).

Fluoride inhibits many metabolic enzymes. Because it interferes with the liver's detoxifying enzymes, it is probably enhancing the effects of other toxic substances in synergistic fashion. The more fluoride we add to the environment, the more toxic other substances may become.

Baby foods and juices should contain no more than 0.01 ppm fluoride. This concentration is the same as that found in human milk (32).

Exposure to fluoride through food, air and water has been increasing for 50 years from many uncontrolled industrial sources and conventional agricultural practices as well as the use of some dental products and medicines. It is imperative that organic foods be kept free of any additional fluoride.

1. Insects. USDA Yearbook 1952. p.220
2. The Merck Index. Twelfth Ed. 1996 entry #8762
3. Crops in Peace and War. USDA Yearbook 1950-51. p.722
4. Soils and Men. USDA Yearbook 1938. p.820
5. 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. ATSDR/TP-91/17.
6. ATSDR, 1993. 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. (<http://www.igc.org/psr/>)
32. Institute of Medicine. 1997. Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D, and fluoride. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board. National Academy Press, Washington, D.C. Page 301-302, 292.

Cite Docket Number: TMD-00-02-PR.

Email Comments to USDA

Note: If you would prefer to send comments by fax, the number is:

703-365-0760

If you would rather send comments by mail, the address is:

Keith Jones
Program Manager, National Organic Program
Room 2945-So.
Ag Stop 0275, P.O. Box 96456
Washington D.C. 20090-6456

Comments due by June 12, 2000

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