Sowing the Seeds of Cancer!
Twenty million tons of phosphate rock contains seven hundred thousand tons of fluorine.
Despite an increasing commercial demand for hydrogen fluoride (HF), the phosphate fertilizer industry has been locked out of the profitable HF market. The fluorine is tied up with silicon and difficult to extract in commercially viable quantities. Commercial supplies of hydrogen fluoride are made from fluorspar mainly imported from South Africa because of the negligible silica content.
In 1993, the Tampa Tribune reported that Bill Erickson, a Polk County, Florida engineer, co-invented a practical process to extract fluorine from silica in phosphate rock.
In 1994, the DuPont Corporation set up a successful pilot plant in Idaho. After a lengthy court battle with the Kaiser Corporation, DuPont was awarded worldwide rights for the process.
HF produced from the new process will be used to make the replacement for ozone depleting CFCs (chlorofluorocarbons), and other products like Teflon, plastics, etc.
Today, many chemists and researchers believe that upon adding fluorosilicate compounds or fluorosilicic acid (water based) to water, the fluoride ion is released and crystalline silica precipitates from the solution. According to that notion, it would be an elementary process to extract the fluorine as HF from phosphate fertilizer production wastewater: Simply add fluorosilicic acid or sodium fluorosilicate to water, siphon off the hydrofluoric acid and leave the silica precipitate. At that point, the hydrofluoric acid could be evaporated, releasing HF gas. However, after processing the phosphate rock into phosphoric acid, and in spite of the commercial demand for HF, most of the fluorine is dumped into evaporation ponds or into drinking water as a fluoridation agents.
The fluorine extraction process invented by Erickson’s company shows that most drinking water fluoridation researchers miscalculated and made erroneous assumptions about how fluorosilicates behave in water. If the process of extracting silica from fluorine were simple as suggested by researchers, phosphate fertilizer companies would have been producing HF for commercial purposes years ago. Selling HF is more profitable than selling toxic industrial waste (sales of the industrial grade fluorosilicic acid do not cover the maintenance or operating costs of pollution scrubbers).
Silicon forms very strong bonds with the fluoride ion. At room temperature, silicon tetrafluoride is a gas; and in the presence of atmospheric moisture, fluorosilicic acid, hydrogen fluoride and silicon oxide gas are created.
Fluorosilicic acid can be distilled into a more pure grade because of the strong molecular bond between silica and the fluoride ion. When the acid is heated, water vapor, HF and gaseous silicon tetrafluoride are driven off and collected as fluorosilicic acid distillate. The attraction between the fluoride ion and silica are so great, even in an alkaline solution of sodium fluoride, the fluoride ion will attack and etch glass.
Various forms of silica such as asbestos and crystalline silica dioxide are considered carcinogenic by industrial toxicologists.
The fluoride ion as the product of USP grade sodium fluoride in distilled water is classified as a probable carcinogen by the National Toxicology Program.
However, it may be possible that silica as a fluoride compound becomes a potentiated or synergized carcinogen and easily metabolized in the body.
Kick Et Al, Fluorine in Animal Nutrition, a 1935, animal study using different types of fluoride compounds showed that fluorine levels in rats fed sodium fluorosilicate 45% more than that of rats fed sodium fluoride. Virtually no fluorine was found in the calcium fluoride group. Urine levels of fluorine in the sodium fluorosilicate group were close to three times those of the sodium fluoride group. Almost no fluorine from the calcium fluoride was found in the urine of the calcium fluoride group. The results of the experiments indicate that sodium fluorosilicate is metabolized at higher levels than sodium fluoride or calcium fluoride. Unfortunately, the researchers did not check for silica levels in tissues, urine or faeces.
|Fluorine Supplement||Time on ration Days||Fluorine ingested Mg||Fluorine in faeces Mg||Fluorine absorbed Mg||Fluorine in urine Mg||Fluorine balance Mg||Fluorine retained %|
|Rock Phosphate (untreated)||11||217.2||128.7||88.5||31.5||+57.0||26.2|
|Rock Phosophate (untreated)||10||213.6||131.5||82.1||20.5||+61.6||28.8|
|Sodium Fluorsilicate (Na1SiF4)||23||269.9||94.3||175.6||93.6||+82.0||30.4|
|Sodium Fluorsilicate (Na2SiF4)||22||269.9||94.4||175.5||90.2||+85.3||31.6|
|Sodium Fluoride (NaF)||18||211.2||116.5||94.7||25.8||+68.9||32.6|
|Calcium Fluoride (CaF2)||11||229.6||225.5||4.1||4.2||-00.1||0.0|
The initial Kick, Et Al experiments were done using pigs as test animals to determine the effects of fluorine in mineral supplements, primarily raw phosphate rock. When the phosphate rock was digested in stomach acid (a process similar to creating phosphoric acid), one of the products was fluorosilicic acid. The phosphate rock was particularly detrimental to the pigs. Kidneys were the primary target organs and upon autopsy showed chronic, parenchymatous nephritis:
“They were pale in color, contracted, and firm in texture, and their surfaces roughened by numerous nodules and depressions. The capsules were slightly thickened, and in some instances, firmly adherent to the surface. Occasionally, small cysts containing a clear or amber colored fluid protrudes above the surface, or were more deeply situated in, the kidney. One section of the cortex appeared reduced in width, and frequently the medulla contained a considerable amount of fat.
“Microscopically the kidneys showed a nephritis with a varying degree of degeneration of the tubular epithelium and, as a terminal result, the replacement of many tubules and glomeruli with fibrous tissue. None of the animals in the sodium fluoride-fed lot exhibited this condition.”
In 1991, a Russian rat study using silicon tetrafluoride gas determined: The chronic influence of silicon tetrafluoride causes polytropic (multiple) effects on the animal organism. In rats, they include changes in the respiratory system, liver, kidneys, nervous system, bone tissue, as well as the enzyme activities, lipid peroxidation process, and the antioxidant system.” They also state that inhalation of silicon tetrafluoride “constitutes a serious threat of acute intoxication” because it “exerts no selective irritative influence on the lungs.”
Silicon, like fluorine, is never found naturally in its elemental form; it is always combined with another element or elements as a compound.
Most silicon compounds that occur in nature are not considered “toxic” in the “classic” biochemical sense of the term (a dose-response relationship), because silicon compounds are poorly absorbed. If they are absorbed, there is no bimolecular transformation into more reactive compounds. However, epidemiological studies done over the past half century have shown that workers exposed to crystalline silica and asbestos (asbestos is a fibrous silica) have higher illnesses and death rates from malignant and benign lung diseases.
Drinking water regulations allow only seven microscopic asbestos fibers in one liter of drinking water (> 10.0 micrometers in length). Aside from radionuclides and arsenic, asbestos is also listed as a carcinogen.
Apart from the more common cancers associated with asbestos workers, lung cancers and mesothelioma, there are “inconsistent” reports of excess cancer mortalities from “cancers of the gastrointestinal system (esophagus, stomach, colon and rectum), laryngeal cancer, kidney cancer, and ovarian cancer.”
Dr. Carl O. Schulz, author of the Silicon and Silicates chapter in Patty’s Industrial Hygiene and Toxicology said, “Although the mechanism by which these compounds cause these diseases is not fully understood, it is abundantly clear that the physical characteristics of the silicon material is the predominate, if not the only, determinate of biologic activity.”
In essence, it is the presence of the silicates, crystalline, molecular or fibrous, in soft tissues that causes health problems; not that silicates are toxic in and of themselves. The National Institute of Health and International Association for Research on Cancer regard silica as a carcinogen based on the results of animal studies.
One of the most obvious manifestations of exposure to crystalline silica is pulmonary edema. However, silica has also been associated with those mystery diseases that that eludes the average doctor’s scope of knowledge:
“The National Conference to Eliminate Silicosis March 23-25, 1997 in Washington DC enjoyed a splendid turnout of over 600 attendees. In my opinion, the conference attention on silicosis to the exclusion of discussion of other silica health effects was very shortsighted. However, I was delighted by the opening remarks by NIOSH Director, Dr. Linda Rosenstock, who pointed out that we now know that silica exposure is a risk factor for several “new” conditions, and that deliberations should be expanded to consider other health problems such as cancer, autoimmune diseases, nephritis and other kidney diseases, and tuberculosis (TB).” (David F. Goldsmith, Ph.D., Public Health Institute, Berkeley, CA)
Other studies suggest that molecular silica may interfere with DNA structure and cause liver, esophageal, lung, and kidney cancers.
In some silica carcinogenicity studies, researchers use free silica derived from reacting fluorosilicic acid with lime (calcium carbonate). They inject the purified molecular silica into the lab animals to induce sarcomas and fibrogenic neoplasms (precursor to cancers). It is also noted in the Silica chapter that precipitates silica dioxide are used in animal model carcinogenicity studies.
Contaminants in phosphate fertilisers
The phrase “Fluoride is the primary pollutant of concern” is found throughout EPA phosphate fertilizer production documents; however, it is easy to hide other contaminants like silica, radionuclides, etc when they are attached to the fluoride ion. Industry counts on this fluoromania to hide the other pollutants by merely using the innocuous term, “Fluoride.” EPA likes to say fluoride particulates and fluorine gases instead of naming individual fluorides.
The most toxic forms of silica are halides (halogenated silicates) and hydrides (hydrogenated silicates).
Silicon tetrahalides and hydrides are extremely toxic by either inhalation or ingestion. Everyone who drinks artificially fluoridated drinking water is exposed to potentially carcinogenic crystalline silicon halides. This is because “all commercial grades of sodium fluoride contain fluorosilicates” (a silicon halide).
In addition, the most used fluoridation agent in the US is fluorosilicic acid (H2SiF6), which is possibly the most easily metabolized form of the silicon halide products.
H2SiF6 is classified as a weak electrolyte, a liquid and miscible in water, meaning that it does not readily break down into its ionic components: the fluoride ion and silicon (silicon dioxide). This means that the complex silicon-fluoride ion may enter the blood stream as a soluble fluoride compound (a complex ion). Consequently, it is possible for the fluorosilicate to enter a tissue, go through a biochemical reaction where the fluoride ion is released and the silicon ion interacts with oxygen and another mineral such as alminum to form a silicate in soft tissue. The embedded silicate would be a fine submicroscopic particle, which has “significant fibrogenic potential” (precursor to cancer).
That submicroscopic, silica particle (molecule) is the potential seed for a cancer as fibrotic tissue develops around it. Depending on the state of health, previous chemical exposures, and genetic disposition, the fibrotic nodule may or may not develop into a cancer.
With the introduction of one milligram of H2SiF6 into the drinking water releases millions of molecular fluorosilicate ions. Even if the fluorosilicate ion dissociates as suggested by EPA and CDC management, millions of silicon dioxide molecules remain as suspended solids. These submicroscopic silica molecules can be metabolized and circulated throughout soft tissues in the body. In contrast, EPA drinking water regulations only allow seven microscopic fibers of less than ten-millionths of a meter (10.0 micrometers) long in one liter of drinking water.
Despite the fact that H2SiF6 and other species of fluorosilicates are potentially carcinogenic, EPA and the CDC National Toxicology Program management suggest that fluorosilicates will behave the same as sodium fluoride in any environment.
As far back as 1934, scientists were aware that not all fluoride salts behave in the same way when ingested.
Kick and associates saw significant differences in absorption rates and toxic effects of different forms of fluorides. More recently, Dr. Arthur Gregory, peer reviewer for the 1993 Toxicological Profile for Fluorides, stated that not all fluoride salts are of the same toxicity. However, no clinical studies have been done using any of the fluorosilicate compounds with regard to use as water fluoridation agents, and/or the effects of long term low-level exposures to these compounds.
The safety or carcinogenic potential from long term low-level exposure to fluorosilicates in drinking water is unknown.
1. The Geology of Florida, University Press of Florida, 1997, pp. 141-144, 247-249
2. Cryolite is calcium fluoride, see Merck Index.
3. Polk firm engineers new technology, Tampa Tribune, April 11, 1995.
4. DuPont Corporation holds the worldwide rights for the process. After a legal battle and appeal, DuPont is beginning to go forward with production. A successful pilot project was established at an Idaho Phosphate fertilizer plant (Telephone interview with Bill Erickson, chemical engineer for the company holding the patent).
5. Denzinger, H.F., König, H.J., Krüger, G.E., Fluorine recovery in the fertilizer industry – a review, Phosphorus & Potassium, no. 103, Sept/Oct. 1979.
6. Gaseous Fluoride Emissions From Gypsum Settling and Cooling Ponds, Howard E. Moore, Florida Scientist, vol. 50, spring 1987, pages 65-78.
7. AWWA Standard For Fluorosilicic Acid, B703
94, AWWA Standard for Sodium Fluoride, Sodium Fluorosilicate, and Potassium Fluorosilicate B703-94.
8. Methods Used and Adopted by the Association of Florida Phosphate Chemists, Seventh Edition, 1991.
9. Phosphoric Acid (H3PO4), www.metalologic.be.MatWeb/reading/acids_acpo4.htm
10. A. W. Frazier, J.R. Lehr, E.F. Dillard, Chemical Behavior of Fluorine in the Production of Wet Process Phosphoric Acid, Tennessee Valley Authority, Muscle Shoals, TVA Bulletin Y-113.
11. Voltaix, Inc. Silicon Tetrafluoride, Technical Information Sheet.
12. See Sodium Fluoride monograph in Merck Index.
13. K. Seppelt, Angewwandte Cheme,31 292 293, Does the Naked Fluoride Ion Exist, Abstract in Fluoride, Vol. 26, April 1993
14. Silica and Some Silicates, International Agency for International Cancer Research (IARC), Monographs on the Evaluation of the Carcinogenic Risks of Chemicals to Humans, Vol. 42, 1987.
15. Maurer, J.K., Chang, M.C., Boysen, B.G., et al. 1990, 2-year Carcinogenicity Study of Sodium Fluoride in Rats, Jour. National Cancer Institute, 82 (13): 118-1126.
16. C.H. Kick, Et Al, Fluorine in Animal Nutrition, Ohio Agricultural Experiment Station, Bulletin 558, Nov. 1935 (deals with phosphate rock fed to farm animals and fluorosilicates), pg. 61.
17. Occupational Diseases, A Guide to Their Recognition, 1977, U.S. Public Health Service (Has not been revised to date).
18. G.I. Rumyansteva et al, Experimental investigation of the Toxic Properties of Silicon Tetrafluoride, Gig Sanit 1991 May
19. Silicon and Silicates, Including Asbestos, Chapter Fifteen, Carl O. Schulz, Patty’s Industrial Hygiene and Toxicology, Vol. II, Part A, 1993, John Wiley and Sons, NY.
20. Drinking water Regulations and Advisories, USEPA Office of Water, 1995.
21. Patty’s Industrial Hygiene and Toxicology, Vol. II, Part A, 1993, John Wiley and Sons, NY.
22. See Sodium Fluoride monograph, 1996 in Merck Index.
23. Monograph for Sodium Fluoride, The Merck Index, An Encyclopedia of Chemicals, Drugs, and Biologicals, Merck Research Laboratories, Merck & Co., Inc. (also see monograph for fluorosilicic acid).
24. Toxic Properties of Inorganic Fluorine Compounds, R.Y. Eagers, 1969, Elsevier Pub. Co., NY.
25. Material Safety Data Sheets for Fluorosilicic Acid.
26. Toxicological Profile for Fluorides, Hydrogen Fluoride, and Fluorine (F), USDHHS, USPHS, ATSDR, April 1993.
27. See Merck Index, Fluosilicic acid monograph: “All commercial grade fluorosilicic acid is a byproduct of phosphoric acid production.
28. According to the Lewis theory, fluorosilicic acid should be classified as a strong electrolyte, but again a fluoride compound seems to be an exception to the rules and acts like a weak electrolyte.
29 International Chemical Safety Cards, ICSC 1233, Fluorosilicic Acid.
30. Fundamentals of Industrial Hygiene, B. Plog, G. Benjamin, M. Kerwin, 1988, National Safety Council.
31. A meter is about three feet. 10.0 micrometers = < 0.0000036 inches
32. M.C. Smith, R.M. Leverton, Comparative Toxicity of Fluorine Compounds, Industrial And Engineering Chemistry, 1934.
33. Saffiotti U, Ahmed N TITLE: Neoplastic transformation by quartz in the BALB/3T3/A31-1-1 cell line and the effects of associated minerals. SOURCE: Teratog and Carcinog Mutagen; 15(6):339-56 1995 UI: 96310605
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