FLUORIDATION, TOBACCO AND POLONIUM-210


The presence of polonium in tobacco smoke
has been known since the early 1960s.

The death of  the Russian former KGB (FSB) agent
Alexander Litvinenko has been linked to the
presence of a ‘major dose’ of radioactive
Polonium-210 in his coffee.

¿ Polonium is NOT subject to IAEA safeguards ?

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Polonium-210 png copy 2The two decay products of uranium:
RADON-222  and  POLONIUM-210 are
considered to be the second leading cause of  lung
cancer and are dangerous and carcinogenic.

The health risks are enormous, including:
bone cancer, internal organs destruction, brain damage and more.
Tobacco companies for 40 years have been concerned about
the public relations and litigation problems posed by
  polonium-210 in cigarettes. 

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Polunium-210 is soluble and is circulated through the body to every tissue and cell.
The proof is that it can be found in the blood and urine of smokers.
The circulating Polonium-210 ⇐ 165 references here] causes genetic damage and early death from diseases reminiscent of early radiological pioneers:

liver and bladder cancer, stomach ulcer, leukemia, cirrhosis of the liver, and cardiovascular diseases.

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     In his 1988 Report of the Surgeon General, it was reported that nicotine has an addictiveness similar to that of heroin or cocaine.
The Surgeon General C. Everett Koop MD (USPHS) stated that radioactivity, rather than tar, accounts for at least 90% of all smoking-related lung cancers.– The Center for Disease Control stated “Americans are exposed to far more radiation from tobacco smoke than from any other source.” 

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“Polonium 210 cancels out tellurium and selenium.
The number one reason for lung cancer is
polonium 210 toxicity causing a selenium deficiency.
The number two reason for lung cancer is the noble gas radon.”
Dr. Richard Olree  - ‘Minerals for the Genetic Code’

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As little as 0.03 microcuries (6.8 trillionths of a gram) of
polonium-210 can be carcinogenic to humans.

Marlboro cigs slop f

Puff  by puff, the poison Polonium-210,
builds up to the equivalent radiation dosage of 300 chest x-rays a year for a person who smokes one and a half packs a day. The presence of polonium in tobacco smoke has been known since the early 1960s.
Some of the world’s biggest tobacco firms researched ways to remove the substance to no avail
—over a 40-year period, but have never published the results
.

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alpha form -polonium

   See more →  Fluoridation and the Phosphate Connection

   Extract:

“…Engineer Thomas Reeves has acknowledged the presence of radionuclides in fluorosilicic acid.

Radon-222 is not an immediate threat because it stops emitting alpha radiation and decays into lead-214 in 3.86 days. Lead-214 appears to be harmless but it eventually decays into bismuth-214 and then into polonium-214. Unless someone knew to look for specific isotopes, no one would know that a transmutation into the polonium isotope had occurred.

Polonium-210, a decay product of bismuth-210, has a half-life of 138 days and gives off intense alpha radiation as it decays into regular lead and becomes stable.
Any polonium-210 that might be present in the phosphate concentrate could pose a significant health threat. A very small amount of polonium-210 can be very dangerous, giving off 5,000 times more alpha radiation than the same amount of radium.
As little as 0.03 microcuries (6.8 trillionths of a gram) of polonium-210 can be carcinogenic to humans.”

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Alexander Litvinenko and Polonium 210

Alexander Livinenko Before & after P.210

The Death Of  The Russian Former KGB (FSB) agent Alexander Litvinenko has been
linked to the presence of a ‘major dose’ of radioactive Polonium-210 in his coffee.
Traces of the radioactive substance were discovered at various locations
in London visited by Mr. Litvinenko as well as in Russia and on two
British Airways (BA) flights.

His body was buried in a lead lined coffin. –  December 2006

FSB Moscow Polonium storeMore  info  → HERE  

Yasser Arafat and Polonium 210        

ArafatYasser Arafat – 24 August 1929 – 11 November 2004             ‎

By Adrian Blomfield, Middle East Correspondent,  03 July 2012 

Tests performed by a laboratory in Switzerland found significant traces of Polonium-210 on the late Palestinian leader’s clothes, adding a new twist to a case that has obsessed the Arab world for years.
Polonium-210 is the same substance used to poison the Russian dissident Alexader Litvinenko in London. (See Above) The claims are likely to renew long-held Palestinian suspicions that the Israeli spy agency Mossad assassinated Arafat, who died in a Paris hospital in November, 2004.

The Institute de Radiophysique in Lausanne found elevated levels of the element on Arafat’s personal effects. A urine stain in his underwear registered a level of 180 millibecquerels of Polonium-210, more than 20 times the dose to kill an average human being. “I can confirm to you that we measured an unexplained, elevated amount of unsupported Polonium-210 in the belongings of Mr Arafat that contained stains of biological fluids,” Dr Francois Bochod, the director of the institute,
told Al Jazeera, the pan-Arab television station.

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WATER FLUORIDATION AND POLONIUM 210

Uranium, Radium and Polonium-210  [ IAEA ] are known carcinogens
which are found in  fluorosilicic acid - used for water fluoridation.
Polonium-210 is one of two decay products of  Uranium…
Polonium decays into stable Lead-206, which also has
significant health risks—especially in children .
Drinking 
fluoridated water increases
lead absorption in our bodies. 

~~~~~~◊~~~~~~

     See – QUT Research by Ross Kieinschmit in Queensland   HERE

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MY VIEWS ON FLUORIDATION – Robert L. Isaacson – Department of Psychology

“Both the very young and the very old are
most likely to be adversely affected
after exposure to fluorides.”

My-views-Isacson   

 Original text →    HERE   ← Thank you Robert

My Views on the Fluoridation of Water

Robert L. Isaacson Distinguished Professor of Psychology Binghamton UniversityA note on terminology: Fluorine is an element in the halogen group as are chlorine and iodine. Of all the known elements, fluorine is the most chemically reactive, most powerful oxidizing, and most electronegative element. It is a stronger oxidizing element than ozone. It reacts with many compounds at room temperature. It is never found in its pure form in nature.Fluoride: Any combination of fluorine with another element or chemical group of elements. Thus, the addition of fluorides to the drinking water can indicate the addition of a large number of chemical agents. The most commonly used fluorides for this purpose are sodium fluoride, NaF, and compounds that contain both fluorine and silicon. Such agents are collectively called “Fluorosilicates.” They include fluorosilicic acid, fluorosilicate, hydrofluosilicic acid, and hexafluorosilicic acid.In 2003 when I accepted an invitation to join the National Research Council’s Committee formed to evaluate the EPA standards for the amount of fluoride that should be allowed in our drinking water, I had no fixed opinion on whether or not fluoride should be added to drinking water. Probably I was asked to serve on the committee because I had organized a series of experiments published between 1993 and 1998 using rats to study the effects of chronic administration of aluminum fluoride in their drinking water. My primary interest was in the effects of aluminum on the brain and behavior. Aluminum fluoride was used because fluoride facilitates the passage of aluminum into the brain. At the time, aluminum was considered by a number of scientists to be an important factor in Alzheimer’s disease. Scientists are still actively investigating this possibility. Our studies had to include the investigation of the effects of the fluoride since the aluminum and the fluoride readily become associated after ingestion. In essence we wanted to know the effects of the aluminum, fluoride, and the aluminum- fluoride complex. 1

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In my more than three years working on the National Research Council Committee I learned about the many influences fluoride has on the nervous system and the brain. I also learned about the variety of ways in which people become exposed to it and the work that had been done in trying to determine if fluorides were a hazard to human health and well being. The results and recommendations of this Committee were published late in 2006.2 Slowly, I came to the conclusion that there were strong experimental and clinical indications that fluorides present health hazards to people in many ways. The more I learned, the more I became convinced that the addition of fluorides to drinking water was, and is, a mistake. Accordingly, I decided to share some of my conclusions with any who might wish to know them. Fluorine-containing compounds can affect every living animal and person. Exposure to fluorides can come from the air, the water, and the foods we eat. Fluoride compounds were long used as insecticides. They were especially effective for ants and roaches. Their containers were always boldly marked as a poison and there were warnings on the label to keep them well away from children. This is mentioned only to note that for many years fluorides have been considered to be major health hazards. In regard to health the total accumulation of fluorine in the body is important. Only about half of the amount of fluorides taken in by a person is excreted. The rest stays in the body. Toxic effects are determined by the amount of fluoride stored in the body, current exposure level, and age at the time of exposure. In addition each person has his or her own tolerance level for fluorides. Once this level is exceeded however, dysfunctions of body and/or brain will occur. How these dysfunctions will be expressed depends on the genetic makeup and past experiences of the person. Another factor

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that helps determine a person’s sensitivity to fluoride is their age. Both the very young and the very old are most likely to be adversely affected after exposure to fluorides. As noted, different people exhibit a wide range of toxic reactions to fluorides. Some people affected by fluorides complain of general weakness and chronic fatigue, others complain of cramp-like pains in the abdomen, or nausea. Still others express toxin-induced effects by diminished vision, headaches, migraine attacks, or pains in muscles and joints. These fluoride effects have been described in books by Leo Spira (1950, 1959)3 and George Waldbott and his associates (1978).4 It is difficult to determine whether or not a given set of symptoms is a consequence of fluoride intake. It is first necessary to rule out the presence of other diseases that could produce the observed symptoms. A correct diagnosis is best shown by repeated observations of an individual when drinking pure water or water contaminated with a fluoride. These exposures must last for periods of a week or two under conditions in which the patient doesn’t know which type of water is being consumed. If the symptoms disappear when the person is drinking pure water and return with the resumption of drinking the fluoride- treated water, this is evidence that the problems arise from the fluoride. Leo Spira and George Waldbott and his associates used this type of experimental approach in their research. Since people vary so much in their sensitivities to fluorides and also in the nature of their symptoms caused by this toxin, determination of a uniform “safe” level of exposure for everyone is impossible. In a way, fluorides are like ozone: there is no really “safe” level that would protect everyone. The Congressional Safe Drinking Water Act instructed that the level of fluoride in drinking water should be set so as to be safe for everyone

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regardless of age or overall health. Increasing the problems that can be induced by fluorine in its different forms is its ability to enhance the effects of other toxins to which we are exposed. For example, fluorides in the drinking water accelerate the absorption of lead, aluminum, and silicon into the body and brain. The toxic effects of lead have been known for hundreds of years. In recent years the focus of attention has been on the learning deficits lead produces in children. The mechanisms proposed for the induction of this effect are not known entirely but there is evidence that many of the most important neurotransmitters of the brain are being affected. These include alterations in dopaminergic, cholinergic, and glutaminergic systems as well as in the “supportive” glia cells of the brain. There is also evidence that lead toxicity may go beyond impairments of intelligence. Indeed, lead toxicity may produce behavioral changes that include loss of impulse control and a related increase in the frequency of violent acts.5 The health hazards associated with enhanced incorporation of lead are not induced by all fluorides but primarily, and maybe only, by the addition of a silicofluoride to our drinking water. The fluoride most often added to our drinking water is hexafluorosilicic acid. This fluorosilicate dissociates when it enters the body. One component contains silicon and another fluorides. As a consequence when silicofluorides are added to our drinking water there are really two toxic hazards: one coming from the fluoride and another from the silicon. Silicon can produce its own toxic effects including the formation of solids (silica and silicates) that can lodge anywhere in the body. In addition the silicon portion also can generate destructive hydroxyl ions in many organs including the brain. The brain damage caused by the production of these free radicals has been related to anti-social behavioral

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actions and violence.6 Recently data from 327 towns and cities, some having fluoridated water and others not, have been compared in terms of crime rates. All the communities with fluoridated water had substantially higher rates than did those with non-fluoridated water. This indicates that fluorides can act to enhance the damage being done by other toxins. The impairment of intelligence from lead toxicity is now well established. It is possible that fluorides can produce negative effects on measured intelligence also. The country devoting the greatest attention to this possibility is China. As of February 2007, several groups of Chinese investigators had published over 20 scientific papers on this topic. Scientists from many different areas of China participated in these investigations. The children studied in these reports ranged in age from 4 to 14. All were tested by the same or very similar standardized I.Q. tests. Overall the results came from children tested at different places, at different ages, and tested by different investigators. All the results from China have found that communities with high levels of fluoride in their drinking water have fewer children scoring at the “bright” end of the intelligence spectrum than communities with low or no level of fluoride. Since China does not fluoridate their drinking water, the Chinese studies compare the I.Q. scores of children from towns and school areas that differ in the amount of fluoride naturally present in their water supplies. While not all of Chinese studies were perfectly designed, the large number of studies showing the same pattern of results calls for our attention. A negative effect of fluoride on intelligence seems to be a possibility. Other studies in China have indicated that fluoride exposure in the drinking water of mothers during the 6th to 8th months of pregnancy can

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produce anatomical changes in the fetal brains. There are also reports of impaired responsiveness to visual and auditory stimuli in babies in the first three days after birth induced by the intake of fluoridated water by young mothers during gestation.7 The ingestion of fluoride tends to increase the uptake of aluminum by the brain. In the studies done in my laboratory the increase in aluminum in the brains of rats was not a function of the amount of aluminum fluoride given the animals in their drinking water. The smallest dose of aluminum fluoride produced about the same amount of aluminum in the brain as a dose 10 or even a 100 times larger. A small amount of fluoride seems capable of opening aluminum pathways to a maximal degree. It is of great interest that the relative risk of having Alzheimer’s disease is increased when individuals had high amounts of aluminum in the brain coupled with low amounts of fluoride.8 Another observation of interest is that aluminum by itself may not exert toxic affects on the nervous system. It may only become a toxin after joined together with a fluoride to become an aluminum fluoride. 9 The chronic administration of fluorides in rats produces changes in the microscopic structure of the brain. There were significant losses of cells in areas of the hippocampus and the neocortex. Many apparently dead or dying cells were found in areas analogous to locations in which similar dying cells are found in the brains of Alzheimer’s patients. A common and, perhaps universal, characteristic of dementia is a reduction of aerobic metabolism in the brain. The blood supply reaching the brain is the primary supplier of oxygen and nutrients. Reductions in this sole source of brain energy can be due to a number of physical or chemical changes. When the brains of animals chronically exposed to aluminum fluoride were examined histologically, deposits of aluminum-based crystals

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were found along the walls of both large and small blood vessels in the brain. Similar deposits were also found in the center of many vessels suspended by collagen fibers. These deposits decreased the normal transfer of oxygen from the red blood cells to the brain since they must have created turbulence in its blood flow. It is of historical interest that Alois Alzheimer, the man for whom a type of dementia was named, noted that most patients with this disorder suffered from atherosclerosis in addition to other brain anomalies. This condition is one in which there are deposits formed on the sides and in the center of arteries in the brain. The deposits disrupt the flow of blood to the brain often cause severe brain damage. Brain functions are entirely dependent on the availability of oxygen. The brain itself consumes 20% of all the oxygen used by the entire body. The brain area most affected by the reduction in oxygen availability is the forebrain. The lower centers of the brain, namely the midbrain and hindbrain, are more resistant to oxygen deprivation. This is why the higher functions of the brain are the first to be affected, as well as the most affected, by oxygen deprivation. Basic motor and visceral functions are often spared even in patients with profound interruptions of normal blood supplies to the brain. One of the best-known chemical alterations produced by fluorides is a reduction in cholinesterases, including acetylcholinesterase. Fluorides also directly affect the actions of many of other important neurotransmitters in the brain. Fluorides seem to have a special attraction to acetylcholine. Nerve cells that synthesize this transmitter have numerous projections to many forebrain areas, including the neocortex and deeper areas of the brain that provide information to the neocortex. Not only do fluorides change the amount of the acetylcholine in the

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brain, they selectively block certain receptors that respond to this transmitter. Fluoride reduces the number of one type of “nicotinic receptors” for acetylcholine. Some other nicotinic subtypes are not affected.10 Added to all of the other alterations in structure and function of the brain caused by fluorides, the opportunity for mental and behavioral changes are almost limitless. While the cholinergic system of the brain has been most studied in regard to the effects of fluoride, it is not the only neural transmitter affected. It is likely that all neural transmitter systems are affected by fluoride intake, directly or indirectly. Other anomalies related to fluoride intake are found in many other chemical systems of the brain. During the period from 1956 to 1963, the endocrinologist, Ionel Rapaport, presented evidence of a link between fluoride exposure and the numbers of babies born with Down’s syndrome, (Trisomy 21). For a number of years the only follow up to his work was in the form of epidemiological comparisons between the number of births of such children both to mothers living in fluoridated drinking water vs. the number of such born to mothers births in or non-fluoridated drinking water areas. The demographics of the two or more areas being compared were not fully taken into account in most of the studies. Maternal ages were also not taken into consideration. Overall, the “follow up” studies to Rapaport’s report were not decisive but none of them failed to rule out his original findings. Furthermore, a determination of fluoride effects using standard epidemiological procedures cannot provide convincing information. This is because it is impossible to find populations virtually the same in all regards except for the amount of fluoride in their drinking water. Another problem arises from the difficulty in accurately determining the number of Down’s

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syndrome children born. Some investigators use the number of birth certificates on which the attending physician notes that the baby had Down’s syndrome. Other investigators use only closed hospital records made sometime later. Still other investigators use both. Neither method is perfect. The use of entries on hospital records would seem to be the most accurate method since physicians seldom enter the nature of possible deformities like Down’s syndrome on birth certificates after delivery. Indeed because of the possibility of making a mistake from delivery, the diagnosis is not often made until a determination can be made by laboratory results. Probably the best collection of relevant data comes from a study of births of children born in two areas of Atlanta, Georgia, as reported by Erickson et al. in 1976. Two different estimates of the number of Down’s children and normal children were presented. One estimate of Down’s syndrome births was made by the examination of copies of birth certificates and the other was based on hospital records. A re-examination of Erickson’s data by Burgstahler11 showed an overall enhancement of Down’s syndrome births to mothers from the fluoridated area. Later, in 1998 Takahashi did a fine grain analysis of data from a number of sources that included the corrected numbers from the 1966 Erickson report.12 In the Takahashi report a clear-cut relationship between fluoride exposure and the number of affected children was found in mothers 30 years of age and younger. Recently, Juan C. Molino13 and I using only data from hospital records found the same age-fluoride-Down’s syndrome birth effect. In his report Takahashi extended the analysis of his data through the use of a regression analysis. He wanted to determine if there could be any dose that would not increase the likelihood of having a Down’s syndrome child. According to his calculations there was no such dose. All doses of

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fluoride caused some enhancement of the likelihood of a woman having such a child. There are other data supporting the idea that fluorides can induce genetic alterations. Evidence indicating biochemical interactions of fluoride with the genetic mechanisms of cell division are presented in the NRC report on Fluoride in the Drinking Water. (See Endnote 2) When the possible benefits and possible dangers of fluoride are considered there really is no comparison. Consider the following: There is no known benefit of adding any form of fluoride to our drinking water. Who would want to increase chances of having a less than perfect child? Who would wish to take a chance on a possible reduction of their own mental capacity? Who would want to have their personality altered by fluoride induced alterations in their brain chemistry? Who would want to increase their odds of developing Alzheimer’s disease? Eliminating the addition of fluoride to our drinking water would remove these possibilities. The cost of doing this is zero. In fact it would enrich the communities now adding fluorides to their drinking water.

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Endnotes Varner, J. A., Huie, C. W., Horvath, , W. J., Jensen, K. F., and Isaacson, R. L. (1993) Chronic AlF3 administration: II. Selected histological observations. Neurosci. Res. Comm. 13:99-104.Varner, J. A., Jensen, K. F., Horvath, W. J. and Isaacson R. L. (1998) Chronic administration of aluminum fluoride or sodium fluoride to rats in drinking water: alterations in neuronal and cerebrovascular integrity. Brain Res., 784: 284-298.Varner, J. A., Horvath, W. J., Huie, C. W., Naslund, H. R., and Isaacson, R. L. (1994) Chronic aluminum fluoride administration. Behav. Neural Biol., 61: 233-241.Isaacson, R. L., Varner, J. A., and Jensen, K. F. Toxin-induced blood vessel inclusions caused by the chronic administrations of aluminum and sodium fluoride. Ann. NY Acad. Sci., 825:152- 166. The final report of the committee was published by the National Academies Press in December 2006, entitled “Fluoride in drinking water.” It can by obtained from the National Academies Press and by special order from any bookstore. The electronic link to the NRC/NAS publication sites:

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1 – 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.http://nap.edu/catalog/11571.html. Spira, L. The drama of fluorine, archenemy, of mankind. Milwaukee: The Lee Foundation for Nutritional Research, 1950, 1959. Waldbott, G. L. Fluoridation the great dilemma, Lawrence, KA: Coronado Press, 1978. Masters R. D., Coplan, M.J. Association of silicofluoride treated water lead with elevated blood lead. Neurotoxicology, 2000. 21:1091-1100. Masters, R. D., Coplan M. J. A dynamic, multifactoral model of alcohol, drug abuse and crime: Linking neuroscience and behavior to toxicology. Soc. Sci. Information, 1999, 38: 591-624. Seavy, J., (2005) Water fluoridation and crime in America. Fluoride, 38:11-22. Du Li. (1992) The effect of fluorine on developing human brain. Chinese Journal of Pathology, 21:218-20. Li Jing, Yao L., Shao, Q-L, and Wu, C-Y. (2004) Effects of high fluoride level on neonatal neurobehavioral development. Chinese Journal of Endocrinology, 23: No.5. Belovjovic, G., Jakovlevic, B. (1999) Aluminum and Alzheimer’s disease. Spr. ArArh. Celok 126: 283-289. Strunecka, A. (1999) Aluminum plus Fluoride: a new deadly duo. Dement. 1: 2- 3. Long, Y-G, Wang, Y-N, Chen, J., Jiang, S-F, Nordberg, A., and Guan, Z-Z. (2002) Chronic fluoride toxicity decreases the number of acetylcholine receptors in the rat brain. Neurotox. Terat, 23: 751-757. Burgstahler, A. W. (1966) Fluoridated water and Down’s syndrome. Long abstract of a report of the 21st Conference of the International Society for Brain Research, Budapest. Takahashi, K. (1998) Fluoride-linked Down syndrome births and their estimated occurrence due to water fluoridation. Fluoride, 31: 61-73. Juan Carlos Molina is the Director of the Ferryra Research Institute at the University of Cordoba, Argentina, as well as holding his distinguished professor position there. He also is a visiting research professor at Binghamton University.

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Disclaimer: The material in this document represents my opinions, unless otherwise noted. The content may be copied in part or in full without permission when used in a not for profit format. When used for other purposes, the permission of the author is required. The document is not intended to provide medical advice but rather for the sharing of knowledge and opinions of the author. Decisions about health advice should be based on a personal one-on-one basis with an appropriate physician.

Robert L. Isaacson
Department of Psychology & Centre for Developmental
and Behavioral Neuroscience
Binghamton University
Binghamton, NY 13902-6000
Phone: 607 777 6764 

R.L.-Isaacson

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FLUORIDE-MAGNESIUM INTERACTION-Polish Research

The greatest practical significance of Mg-F– interaction however,
seems to be in processes of bone and tooth mineralization
and in the formation of uroliths.

f-mag_-interaction-sA Machoy-Mokrzynska (Institute of Pharmacology and Toxicology,

pomeranian-uni-poland

Pomeranian Medical Academy, Szczecin, Poland)
The Pomeranian Medical University has more than 500 faculty and
almost 200 technical staff. Among the academic staff are
43 professors and 54 habilitated doctors.
Since 1948  8060 physicians and
3314 dentists graduated from the University.
1113 researchers obtained the degree of doctor
and 196 of habilitated doctor. 

Fluoride (J. of the International Society for Fluoride Research),

Vol. 28 No. 4; November, 1995, pp 175-177

It has now been fifteen years since Marier drew attention to the significance of magnesium in biological interaction with fluorides. (1) The toxic effect of fluoride ion plays a key role in acute Mg deficiency. The amount of F- assimilated by living organisms constantly increases, and Mg absorption diminishes as a consequence of progressively advancing industrialization. Marier gives examples of such retention of both elements in plants (e.g. in pine and tomatoes) and in animals, for instance in bone tissue, blood and kidneys, with the last being thought as the most probable place of Mg-F- interaction.(1) Now, further facts have been observed, which throw a new light on the effects of Mg-F- interaction.

The significance and distribution of Mg in living organisms are widely known and described in textbooks.(2) Fluoride ion clearly interferes with the biological activity of magnesium ion.(3) Present-day Mg deficiencies in humans are the result of intensive expulsion of this element (e.g. under the influence of extensive drinking of alcoholic beverages) or reduced Mg content in the diet, caused, for example, by inappropriate agricultural practices or effects of ecotoxins.(4)

One of the prime locations of possible F- and Mg interactions is the intestines. The increased F-supply reduces intestinal Mg resorption, owing to high chemical affinity of both elements and production of MgF+ and MgF2.(1) However, there are many facts to be considered, since there is a common mechanism of transportation of both these elements through the intestinal walls. Distinct F--Mg interaction is also observed in other cells and tissues. Mg deficiency in plants may limit synthesis of chlorophyll, on which photosynthesis depends. Therefore, supplementation of Mg protects plants against toxic effects of fluoride compounds.(1) Mg deficiency in animals reduces production of energy, relevant to the Mg-ATP system. Reduction of ATP levels affects in an unfavourable way many metabolic processes connected with the action of ATP (eg, metabolism of carbohydrates, proteins, nucleic acids, lipids, and active transport).

The role of Mg and F- ions in enzymology is also well known. Magnesium-dependant enzymes compose the biggest group in enzyme systematics. Magnesium is the activator of more than 300 enzymes, while fluorine is known as their inhibitor, although the activity of some enzymes is known to be increased by fluorine.(5) In general, Mg-F- interactions most frequently decrease enzymatic activity.(6) The greatest practical significance of Mg-F- interaction however, seems to be in processes of bone and tooth mineralization, and in the formation of uroliths.(7,8)

In bone tissue magnesium stimulates the transformation of immature (amorphic) bone into a more crystalic form. Owing to the translocation of Mg into mineral tissue, bone elasticity increases to help prevent fractures. Rats on diet poor in Mg display significantly higher content of F- in femurs and molars. This is undoubtedly related to the assimilability of both elements. Since bioavailability of Mg and F- depends on their mutual ratio in the diet,(9) a low-magnesium diet distinctly increases F- absorption in the intestines.

Taking into account the mineralization of bone tissue, one also cannot ignore the role of calcium. The basic inorganic compound of bones is hydroxyapatite, containing calcium phosphate. The far-reaching antagonism between magnesium and calcium affects not only their different distribution in tissues, but also their mutual dislodging from cells. For example, magnesium favours blocking of calcium channels, disturbs oxidative phosphorylation, intensifies bone decalcification and increases muscle-cell diastole, while calcium intensifies contraction. On the other hand, hypercalcemia enhances Mg loss or magnesiuria.(10)

Mg-F- interaction processes relating to enamel and its effect on caries have also been investigated. Fluoride ion affects enamel hardening (11, 12) and prevents its annealing, but this effect diminishes after administration of Mg. Magnesium alone does not visibly affect tooth plaque, erosive enamel damage, or the course of caries, but Mg and F- administered jointly influence enamel hardening and reduce caries significantly, as demonstrated in rats.(13) In interactions of F- with Mg and Ca, it should be stressed that it is calcium rather than magnesium that intensifies mineralization processes.

Urolith formation is considered to be pathological. Mineral content analysis of uroliths shows that they always contain Mg and F- (besides phosphates, calcium and other inorganic and organic components).(8) Formation of uroliths follows crystallization rules. Mg ion reduces the rate of superficial crystal nuclei formation, whereas F- ion accelerates the process. The former reduces and the latter accelerates growth of calcium phosphate crystals.(7) In the formation of uroliths, calcium is the promotor, and magnesium plays the role of the inhibitor.

It also should be pointed out that uroliths always contain more Ca than Mg. Fluoride on the other hand, favours formation of uroliths and accelerates their production.(8)

In summary, it can be stated that in intoxication with fluorine compounds, magnesium plays a protective role by countering and reducing the toxic effects of F-.


References:

1 Marier J R. Observations and implications of the (Mg F) interrelations in bio-systems: a review and comments on magnesium intake and fluoride intake in the modern-day world. Proceedings of the Finnish Dental Society 76. 82-92, 93-102, 1980. (Abstracted in Fluoride 14, 142 1981).

2 Durlach J. Le magnesium en pratique clinique. Editions Medicales Internationales. Paris 1991.

3 Guminska M. The effect of magnesium on metabolism in living organisms and medical consequences of its deficiency in man. Folia Medica Cracoviensia 26 1-2, 5-28, 1985.

4 Markiewicz J. Environmental factors decreasing magnesium content in alimentary chain. Folia Medica Cracoviensia 26 1-2, 5-28, 1985.

5 Strochkova L S, Zhavoronkov A A. Fluroide as an activator of enzymatic systems. Fluoride 16, 181-186 1983.

6 Chlubek D, Machoy Z. Significance of the effect of fluorine dose on enzymes activity in vivo and in vitro studies.Bromatologia i Chemia Toksykologiczna 22 3-4, 235-242, 1989.

7 Okazaki M. Mg2+-F- interaction during hydroxyapatite formation. Magnesium 6 (6) 296-301, 1987.

8 Machoy P, Bober J. Fluorine-constant component of urinary calculi, Environmental Sciences 2 1 11-15, 1993.

9 Cerklewski F L. Influence of dietary magnesium on fluoride bioavailability in the rat. American Insitute of Nutrition 117 (3) 456-500, 1987.

10 Machoy Z. Biochemical mechanisms of fluorine compounds action. Folia Medica Cracoviensia 28 1-2, 61-81, 1987.

11 Collys K, Slop D, Coomans D. Interaction of magnesium and fluoride in the rehardening and acid resistance of surface-softened bovine enamel in vitro. Magnesium Trace Element 9 (1) 47- 53, 1990.

12 Luoma A R, Luoma H, Raisanen J, Hausen H. Effect of magnesium and fluoride on the fermentative dissolution of enamel by a streptococcal layer as measured by mircrohardness tester and a proton probe microanalysis. Caries Research 17 430-438, 1983.

13 Sorvari R, Koskinen-Kainulainen M, Sorvari T, Luoma H. Effect of a sports drink mixture with and without addition of fluoride and magnesium on plaque formation, dental caries and general health of rats. Scandinavian Journal of Dental Research94 483-490, 1986.

FLUORIDE:

published by the International Society for Fluoride Research Editorial Office:

81A Landscape Road, Mt Eden, Auckland 4, NZ

Subscription Rate: $40. U.S. Funds per year (quarterly publication)

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 see also 

FLUORIDE AND THE ZINK LINK — Leo Spira

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↓  Local information and supplier ↓

More info on Magnesium and Health

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FLUORIDE THE AGEING FACTOR – The Book

 

J.A.-Yia...

     FLUORIDE THE AGING FACTOR  

by

Dr. John Yiamouyiannis

Dr. John Yiamouyiannis was, until his death in the fall of 2000,

the world’s leading authority on the biological effects of fluoride.

His formal education included a B.S. in biochemistry from the

University of Chicago and a Ph.D in biochemistry from the

University of Rhode Island. After a year of postdoctoral research at

Western Reserve University Medical School, Yiamouyiannis

went on to become biochemical editor at Chemical Abstracts Service,

the world’s largest chemical information center.

It was at Chemical Abstracts Service,

where   Yiamouyiannis  ← watch Part 1

became interested in the   damaging effects of fluoride.  ← watch Part 2

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FLUORIDE DEATH CERTIFICATE AND LETTERS +

“…I took him to the doctor straight away and he gave our son a stomach
pump treatment. The doctor told me he could only find four
tablets in his stomach. I was told to take him home and
he would sleep for a while, but he would
be okay when he woke up…”

The Burtons framed m copy

JasonPaulBurton

Copy of Fluoride Death Certificate

Death Cert Jason new extract

lettter from Burtons

See original below ♥

My husband and I have agreed on writing this letter in the hope that it may prevent someone going through the experience we suffered in May 1973.

In July 1970 we were told by our doctor that we were going to have a baby.  In my first visit to the Hospital for a check-up in October, I was told by the Matron to start taking fluoride tablets for the benefit of the baby.  I did so until the 20th of February 1971 when our first child, Jason, was born.

When he was one year old the welfare clinic told me to start giving him 1/2 of a fluoride tablet per day.  I did so for 15 months.  When he was 27 months old he got hold of the fluoride tablets, and at the time I didn´t know how many he had eaten, but I knew it wasn´t many.

I took him to the doctor straight away and he gave our son a stomach pump treatment.  The doctor told me he could only find four tablets in his stomach.  I was told to take him home and he would sleep for a while, but he would be okay when he woke up.  This was at 2:00 P.M.

At 5:30 P.M. I realized that something was wrong, as I couldn´t wake him.  I rang the doctor and was advised to take him back to the surgery.  The doctor saw him staright away and told me to take him to the maternity hospital.  As we arrived he was still unconscious and he stopped breathing.  The doctor put him in a respirator immediately.

The doctor and the nurses didn´t believe that he could be so ill from taking fluoride tablets until they did some test on him.  They told us it would take 200 to 500 tablets to make him so sick.  There were less than 100 tablets in the bottle before he touched it. On May 15th, five days after admission, Jason passed away. The doctor verified that his brain, due to fluoride poisoning, was completely dead. We have now two children.  They have never or will never receive fluoride tablets from us.

We are completely against fluoridation of drinking water and we hope that this letter
will help stop such a thing from happening.

Mr. and Mrs. A. Burton

Birkdale, Brisbane

Queensland, Australia  [4159]

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Hospital Report – (“Discharge Summary”)

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   The FDA Issued Warning Letter to 
Pharmaceutical Company on Fluoride...

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These fluoride tablets were sold in a plastic container
that did not have a “Child-resistant closure”  
- not even a screw top – just a press fit.

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      ♥

 


Burton letter hand 1

Burton letter hand2

Burton letter hand 3

Burton letter hand 4

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More info  →  HERE

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Thais has black teeth

The Ancient Romans knew ‘IT’ damaged teeth and
they knew ‘IT’ was something in the water.

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FLUORIDE KIDNEY DAMAGE

“People with kidney impairment have a
lower margin of safety for fluoride intake.
Limited data indicates that their fluoride
retention may be up to three times normal”

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Fluoride Is A Developmental Nephrotoxin –
Coming To A Kidney Near You

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FLUORIDE AND KIDNEY DAMAGE

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Indigenous-Aus.-s 

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People With Kidney Impairment Are At Greater Risk From Fluorides.

Indigenous Australians have smaller kidneys than non-indigenous Australians –

a reduced number of nephrons and decreased renal reserve –

(Singh G, White A, Spencer J, Wang Z, Hoy W [1999]).

Indigenous Australians are 6 times more likely than other Australians to be receiving dialysis or to have had a kidney transplant. Death rates from chronic kidney disease are 7 and 11 times as high for non-indigenous males and females respectively.

Australia’s peak medical advisory body, the Australian Government’s National Health & Medical Research Council (NHMRC) advised in their Australian Drinking Water Guidelines 2004 that:

“People with kidney impairment have a lower margin of safety for fluoride intake. Limited data indicates that their fluoride retention may be up to three times normal”

Indigenous Australians have high rates of kidney disease and also diabetes, (6 times higher than for non-Aboriginal Australians) which can lead to kidney disease, they are less able to cope with fluoridation, they will have higher plasma fluoride levels, and circulating for longer will accumulate more fluoride in their bodies (particularly bones) because of their decreased ability to excrete fluoride.

BAD YINGAY

The Queensland Government’s proposal to fluoridate indigenous communities, some of which are currently using underground water of untested levels of existing natural fluoride, can be described as reckless stupidity – genocidal, and needs to be reversed immediately.

Inorganic fluoride. Divergent effects on human proximal tubular cell viability. R. A. Zager and M. Iwata. Fred Hutchinson Cancer Research Center, Seattle, WA …

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Inorganic fluoride. Divergent effects on human proximal tubular cell …

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Fluoride, Cadmium, Arsenic – Chronic Renal Failure/Sri Lanka

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“FLUORIDE POLLUTION AND ITS EFFECT ON WATER
AND VEGETATION IN BIRBHUM DISTRICT, WEST BENGAL”

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U.S.A. SURGEON GENERAL WARNS
AGAINST FLUORIDATED WATER IN KIDNEY MACHINES – March 1969

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THE NATIONAL KIDNEY FOUNDATION (USA)

NO LONGER ENDORSES FLUORIDATION:

“The 1981 NKF position paper on fluoridation is outdated.
The paper is withdrawn and will no longer be circulated,
effective from the 10/06/07″ – NKF Board of Director’s meeting.

http://ndt.oxfordjournals.org/cgi/content/full/gfm663v1

      The safety margin for exposure to fluoride by renal patients is unknown, measurements of fluoride levels are not routine, the onset of skeletal fluorosis is slow and insidious, clinical symptoms of this skeletal disorder are vague, progression of renal functional decline is multifactorial and physicians are unaware of side effects of fluoride on kidneys or bone. 

The Nephrology Dialysis Transplantation is a monthly peer-reviewed medical journal. It is published by Oxford on behalf of the European Renal Association (ERA) and European Dialysis and Transplantation Association (EDTA). It is abstracted and indexed in PubMed/MEDLINE/Index Medicus. According to the Journal Citation Reports, the journal has a 2011 impact factor of 3.564.[1] The journal’s current editor-in-chief is Carmine Zoccali from Italy.

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Water Fluoridation Targets Black Americans

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Posted by admin on Wednesday, 12 May 2010

WATER FLUORIDATION TARGETS BLACK AMERICANS

Silicofluorides and Higher Blood Lead

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At present, U.S. public water systems serving over 140 million people are fluoridated with 200,000 tons of commercial grade hydrofluosilicic acid (H2SiF6) and sodium silicofluoride (Na2SiF6), together called “silicofluorides” (or “SiFs”).

Data from numerous studies show that, taking economic, social and racial factors into account, where silicofluorides are used, children absorb more lead from the environment, and there are higher rates of diseases and behavioral problems associated with lead poisoning (including hyperactivity, substance abuse, and violent crime).

Although some early studies showed differences between sodium fluoride and sodium silicofluoride, to this day the substitution of silicofluorides in public water treatment facilities HAS NEVER BEEN SUBJECTED TO APPROPRIATE ANIMAL OR HUMAN TESTING. Recently, the Assistant Administrator of the EPA admitted to Congress that his agency had no data on SiF toxicity and the Chief of the Treatment Technology Evaluation Branch at the National Risk Management Research Laboratory confirmed that the EPA has “no” data on the “health and behavioral effects of fluosilicic acid.”

Despite claims of safety by oral health officials, laboratory research in Germany revealed that silicofluorides do not dissociate completely and have important biological effects. To follow up on this issue, we have compared children’s blood lead levels in communities using SiF treated water with communities using sodium fluoride or with non-fluoridated water. In three separate samples, totaling over 400,000 children, SiF treated municipal water is ALWAYS significantly associated with increased blood lead levels in children.

This effect was evident in a Massachusetts survey of lead levels in 280,000 children (see graph for children exposed to SiF from the Greater Boston water system, from towns that add SiF locally, or from communities using sodium fluoride, and towns without fluoridation). For the state of New York, data was available on venous blood lead levels for 151,225 children in communities of 15,000 to 75,000. Controlling for other factors associated with higher blood lead, silicofluorides were again significantly associated with higher uptake of lead from the environment. For black children, who are especially at risk for high blood lead, those in towns using SiF were less likely to have low blood lead and more likely to have lead over 10µg/dL. To confirm that these results are not due to other socio-economic or demographic factors, additional statistical tests were run.

The third study concerned children’s blood lead levels in the National Health and Nutrition Evaluation Survey (NHANES III), which had reports for 7224 children from 80 counties with populations over 500,000. Since only 4 of these counties had any communities that used sodium fluoride, analysis of the NHANES III data focused on the percentage of the entire county population exposed to silicofluoride treated water.

Among the 1543 children of all ages from large urban counties with over 80% of the population exposed to fluoridation (almost all of whom receive water treated with SiF), average blood lead was 5.12 µg/dL whereas the average for 1139 children in low fluoride exposure counties was 3.64 µg/dL Blood lead in the 473 children sampled from the medium fluoridation counties was 3.23 µg/dL, which was significantly different from the high fluoridation counties but not from either low fluoridation counties or those with unknown fluoridation status, where average blood lead levels were 3.16 µg/dL (S.D. 2.83). Controlling for the Poverty, the effect of SiF use was highly significant (p < .0001). When the sample is divided by age and race, these findings provide six separate samples in which SiF is associated with high blood lead (see Graphs).

In all three populations studied, those children in each racial category and each age group who were highly likely to be exposed to silicofluorides differ strongly in levels of blood lead from those not exposed.

This conclusion was further checked by analyzing available data for health and behavioral traits that have been associated with high blood lead (such as violent crimes, cocaine use and asthma). In each case, those exposed to silicofluoride treated water were more likely to have behavioral or health problems that are more likely among those with high lead in their bodies.

The injection of silicofluorides in public water supplies is a practice whose elimination could possibly contribute to reduced rates of learning disabilities, substance abuse, violent crime, and asthma (all connected with lead poisoning and other toxins). Whatever the benefits to teeth (and this is highly controversial), our research shows that the issues facing the public concern silicofluoride chemistry, toxicology, and the linkage of neurotoxins with behavior or health. Before SiF chemicals are used, citizens must know that they are safe for all.

 

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40TH PARLIAMENT

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People Are Drinking More Bottled Water

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The Social Implications of Neuroscience: Linking Brain Biochemistry and Violent Crime

On the same topic:

THE PINEAL GLAND

A Short Selection Of Comments

From Famous Researchers

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With special thanks to Rodger D. Masters.

THE SOCIAL IMPLICATIONS OF NEUROSCIENCE:

LINKING BRAIN BIOCHEMISTRY AND VIOLENT CRIME

Roger D. Masters (Dartmouth College)·

THIS FILE IS A DRAFT OF THE CHAPTER WITH THIS TITLE IN:

Richard W. Bloom and Nancy Dess, eds.,

Evolutionary Psychology and Violence:

A Primer for Policymakers and Public Policy Advocates

(Westport: Praeger, 2003), pp. 23-56.

ABSTRACT

It is impossible to deny that a revolution in neuroscience and other areas of biology has taken place over the last half-century.  The  estimates of 83 million Americans taking drugs like Prozac for depression and 11 million children on Ritalin for hyperactivity indicate it is time to reconsider the role of brain chemistry in social behavior and violent behavior.  Since it is obvious that loss of impulse control can contribute to violent outbursts – and evidence shows that some toxic chemicals (such as lead) can have this effect, it is time to consider neuroscientific evidence linking environmental toxins and rates of violent behavior.  To illustrate the implications of the new issues involved, I focus on a hitherto unexplored example.  Two chemicals (H2SiF6 and Na2SiF6, jointly called “silicofluorides” or SiFs) are used to treat public water supplies of 140 million Americans even though, as the EPA has admitted, they never been tested for safety.  To illustrate the interdisciplinary complexities entailed when linking brain chemistry to policy decisions concerning violent crime, our argument has four main stages: first, why might SiFs be dangerous? Second, what biochemical effects of SiF could have toxic consequences for humans?  Third, on this basis a research hypothesis is formulated to measure the types of harm.  In this case, we predict children in communities using SiF should have increased uptake of lead from environmental sources and higher rates of behavioral dysfunctions such as hyperactivity (ADHD) known to be caused by lead neurotoxicity.  Finally, the hypothesis is tested using multiple sources of data including rates of violent crime studied using a variety of multivariate statistical techniques (including analysis of variance, multiple regression, and stepwise regression).  As this outline should make clear, a combination of interdisciplinary perspectives and great prudence is needed to link research in neuroscience to policies concerning violent crime,  If confirmed, however, the potential benefits of hypotheses like the one tested below may be great, revealing the generally unsuspected value of including neuroscientific research in the analysis of human social behavior.

Requests for reprints and correspondence should be directed to: Prof. Roger D. Masters, Department of Government, HB 6222, Dartmouth College, Hanover, NH 03755. Email:  Roger.D.Masters@Dartmouth.edu

The full version of the above is on the net,

and as the above suggests adding silicofluorides

to drinking water amounts to domestic terrorism.

 Editor’s note:

Zinc deficiency can account for bad behaviour – F. is an antagonist of zinc.

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Fluoride and Crime in the USA

Original  →  HERE

SUMMARY:

A four-part study explores possible connections between 

water fluoridation and crime in America.

Part A, Media-reported crime database and fluoridation, presents an observational database of violent crimes, mostly multiple shootings, and finds an unusually high percentage of them associated with water fluoridation, suggesting the existence of a “fluoride-related” category of crime. A low-end threshold for the toxic effects of fluoridation of 0.3 ppm is identified, and the term “fluoridated” is defined here as having a fluoride level of 0.3 ppm or higher. In Part B, Online crime database and fluoridation, a published database of year 2000 crime data for 327 US cities over 75,000 population, representing 80 million Americans, was expanded to include fluoridation data for these cities. Water fluoridation was consistently associated with high crime rates at all population levels. Part C, Book crime database and fluoridation, examines year 2000 crime statistics for six major crimes in the same 327 cities according to their fluoridation status. Cities having natural fluoridation, or which use silicofluorides or sodium fluoride, are shown to have substantially higher crime levels than nonfluoridated cities. Part D, Lead related crime, quantifies the amount of crime historically associated with lead intoxication, thus identifying a remainder which may be associated with fluorides. This study presents a data-backed hypothesis about one possible cause of crime; it is not a definitive statement about crime causality.

Keywords: Crime; Fluoridation; Fluoride toxicity; Lead toxicity; School shootings; USA.

INTRODUCTION

In 1999 I observed that nine of ten randomly-selected school shootings in America had occurred in fluoridated communities, and that the shooter in the tenth had used Prozac, a fluorinated pharmaceutical.b With less than 60% of the U.S. population fluoridated, a non-random correlation between fluoride and violence was suspected.

Others have connected fluorides with violence. Grandjean et al identified significantly elevated mortality due to violence and suicide among Danish cryolite workers.1 Several studies have examined effects of fluoride on mental development, brain function, and behavior. Li et al, Zhao et al, and Xiang et al showed that high fluoride exposure reduces intelligence in children.2-4 Varner et al documented the effects of aluminum fluoride and sodium fluoride with neuronal damage, dementia, and mortality in rats.5,6 Mullenix et al documented detrimental CNS effects of sodium fluoride in rats, showed that timing of fluoride (a).

Correspondence: Jay Seavey, AIA emeritus, P.O. Box 5234, Manchester, NH, USA 03108-5234. E-mail: jayseavey1618@earthlink.net bKip Kinkle murdered his parents, then killed 2 and wounded 22 in a school shooting on 5/21/98 in unfluoridated Springfield, OR. The police report indicated that he had previously been treated with Prozac [fluoxetine hydrochloride]. A structural formula for Prozac appears in Physicians’ Desk Reference, 53rd ed., Montvale NJ: Medical Economics; 1999. p. 924. The other nine fluoridated locations noted at the time were: Moses Lake, WA; Bethel, AK; Pearl, MS; West Paducah, KY; Jonesboro, AR; Edinboro, PA; Fayetteville, TN; Littleton, CO; and Taber, Alberta, Canada. My observations were made at a public hearing on fluoridation held in Manchester, NH, and reported in The Union Leader (Manchester, NH)1999 Sept 23, Sect. A:1,20.

 Fluoride 2005;38(1)

12 Suavely [?] exposure can be developmentally critical, identified sex-linked differences in some of these effects, and demonstrated fluoride accumulation in the brain.7 Others have explored heavy metal intoxication with and without fluorides, and their mental and behavioral effects. Needleman et al showed psychological impairment and behavioral deficits in children from lead exposure.8 Masters and Coplan focused attention on elevated blood lead levels when silicofluorides are used for water fluoridation.9 Other work by Masters et al addressed manganese and lead toxicity, and silicofluoride use, relative to crime, alcoholism, and cocaine/crack abuse; and identified a time lag between the removal of lead from gasoline, and a later decline in crime rates.10 Fluoride, by itself and in conjunction with heavy metals, appears to alter brain function and to predispose some humans to violence. It seemed timely to study more directly the relationship between fluoridation and crime: cumulatively, these earlier studies led to an expectation that such a relationship could be demonstrated.

The work reported here is divided into four parts, A, B, C and D. They evolved sequentially over about four years, and do not reflect a methodology adopted from the outset.

MATERIALS AND METHODS

Part A: Media-reported crime database and fluoridation

Stories were accumulated from news mediaa over a period of approximately two years and assembled into a database (“A”) of 152 events, most of which occurred between 1993 and 2001 (media stories sometimes reported sequelae, such as court proceedings). The stories were primarily of multiple shootings, but also included unexecuted events involving weapons and similar ideation. The database also included some stabbings, drownings, arsons, and bombings, the

A The collecting of news stories utilized The Union Leader (Manchester, NH), and America Online; many of the stories from these sources originated from The Associated Press or from Reuters. The stories were selected, based on their content and on my intuition, from my routine daily reading, rather than from a methodical or exhaustive search using, for example, keywords or search engines. Events were typically multiple murders, usually with firearms, having an apparent “senseless” character to them. Events with known motives (except crimes grossly disproportionate to their motives), or which were known to be gang-or drug-related, were excluded. Domestic violence was excluded unless the victims included children. Stories were typically clipped, or were downloaded and printed, and placed in a file; periodically, the file would be reviewed, and the fluoridation status of the locations and of the perpetrators would be determined using the Fluoridation Census 1992. American Automobile Association roadmaps for the entire United States were regularly consulted to gain information about locations mentioned in news stories. In many cases telephone calls were made to get detailed information about local water systems. Calls were also made, with far less success, to get information about perpetrators and their life histories. Law enforcement personnel were generally reluctant to divulge much in the aftermath of an event, while it was still being investigated. Efforts to gain information from news writers were equally fruitless. In many instances, a succession of news stories over a period of time was needed to extract basic information about an event, as the initial reporting about a multiple shooting might be sketchy. On several occasions, after a major event, the news sources carried a list of 10 or 15 similar events—school shootings, workplace shootings, etc. These event lists, if they included events I had not already listed, were typically searched out using the Internet. This, along with current reporting of event sequelae [squealed], such as court proceedings, provided an avenue for including events going back several years. These lists also provided a basis for comparison: by the time I had accumulated 152 events, the database was more inclusive, by a factor of ten, than the longest of these lists which the media had presented; yet it is by no means deemed to be exhaustive.

Fluoride 2005;38 (1)

Water fluoridation and crime in America 13 common denominator being the heinous and senseless character of the crimes, and an absence of apparent motive. In each case, after an event was identified for inclusion in the database, a search was later made to determine the fluoridation status either of the place where the event occurred, or of the place where the perpetrator lived. A fluoridated community is defined for this study as one having a fluoride level of 0.3 ppm or more in the public water supply.a A statistical analysis was then performed, comparing the “fluoridation-connection” of the collected events with the nationwide fluoridation level. As a control, database “B” was developed, utilizing 164 randomly selected stories published between 1993-2001 in “The Armed Citizen”, a regular column in American Rifleman, a monthly magazine published by the National Rifle Association. These stories reported incidents in which firearms were used by citizens for self-defense.

Part B: Online crime database and fluoridation

Noting that Part A was somewhat limited by the particular type of crime it focused on, I broadened the search to include publicly-available data on a wider category of crimes. A database by Morgan Quitno Press (MQP), Lawrence, Kansas, published in book form and posted online, listed crime data for the year 2000 for 327 American cities having populations over 75,000, and rated their comparative safety according to a score or index which represented their aggregate incidence, based on FBI crime statistics, for six major crimes: murder, rape, robbery, aggravated assault, burglary, and motor vehicle theft.11,12 The score for each of the 327 cities was referenced to a national average of 0.00, and

aThe U.S. Public Health Service has generally defined “fluoridated” water as having a fluoride level at or above 0.6-0.7 ppm. The reason for selecting a lower level of 0.3 ppm to define “fluoridated” for the purposes of this study is as follows: Human physiology has some capacity for detoxifying and eliminating fluorides. Dental fluorosis offers the most readily-available and visible indicator for fluoride intoxication. Therefore, if we can establish a level below which this toxicity is not evident, it provides at least a speculative basis for considering that other toxic effects we are hypothesizing about may also not manifest themselves below this level. In other words, we are not interested in a level above which some hypothetical dental benefit allegedly occurs; we are concerned, rather, with the level below which toxic effects are not in evidence. H. Trendley Dean, DDS, in “Epidemiological studies in the United States” (In: FR Moulton, editor. Dental Caries and Fluorine. Washington, DC: American Association for the Advancement of Science, 1946. p. 5-31.) provides data from America necessary to make this determination. While Dean does not identify 0.3 ppm as a definitive cut-off level for the appearance of dental fluorosis, his tabulated data in Table XI, page 23, show that the prevalence of dental fluorosis begins to rise sharply above a fluoridation level of 0.3 ppm, and that the few observed cases occurring below this level are characterized as “very mild”. The appearance of dental fluorosis probably does not hinge solely on fluoride in drinking water; it probably reflects nutrition in general, and the mix of other minerals in the drinking water. Fluoride exposure relates partly to diet, being high, for example, in a diet high in seafood. The toxic manifestations of fluoride, it is believed, are also reduced by activities which remove fluoride from the system, such as hot-water bathing or sweat bathing. There is a discussion in Fluoridation: The Great Dilemma (Waldbott GL, Burgstahler AW, McKinney HL. Lawrence KS: Coronado Press, 1978. p. 180), of significant levels of dental fluorosis on the South Atlantic island of Tristan da Cunha, where the fluoride level is 0.2 ppm. This, however, seems to be the extreme end of the spectrum, and it may reflect a diet high in fish, but possibly relatively deficient in Vitamin C, calcium, and/or magnesium. For all of these reasons, but particularly on the basis of Dean’s American data, 0.3 ppm and above was chosen to define the term “fluoridated”. It is not suggested that fluoridation levels below 0.3 ppm have no toxicity, or that this represents a “safe” level of fluoride in water.

Fluoride 2005;38(1)

14 Seavey

scores ranged from –84.94 (safest) to 373.28 (most dangerous). The MQP database for its “Safest Cities Award” includes nearly 80 million Americans—about 28.5% of the U.S. population. a I modified this database by adding fluoridation data for each of the 327 cities, and then sorted the list into six groups by population size. Within each group, cities were listed according to increasing “score” or “crime index”. Each of the six groups was then bifurcated, to identify a Low Crime subgroup and a High Crime subgroup within each population group. Total fluoridation incidence for each of the six population groups was determined, and its percentage was calculated. These percentages determined the expected fluoridation incidences for the Low Crime and High Crime subgroups within each population group. Expected incidences were then compared with observed incidences for each of the 12 subgroups, and the differences were noted. (See Table 1.) A two-way table of the differences was developed, and the chi-squared statistic was calculated. (See Table 2.)

Part C: Book crime database and fluoridation

MQP does not tell us in City Crime Rankings, 8th edition, what formula was used to generate scores for its “Safest City Award.” While these scores are said to allow a direct comparison of cities on the basis of their crime rates, we are not told how these scores or crime index figures can be translated into actual crime rates, and thence, using population data, into actual numbers of crimes. For this reason, I have used MQP’s more detailed published crime rate data, to develop this information.13 For each of the 327 cities, actual year 2000 rates for each of the six major crimes were entered and then totaled into an aggregate crime rate for each city. Fluoridation data were then entered for each city. The 327 cities were then sorted in database “327” according to their fluoridation status. Within each of the fluoridation categories, the cities were sorted by ascending aggregate crime rate.

Part D: Lead related crime

The connection between lead intoxication and criminal behavior appears to be well established.9 The phase-out of leaded gasoline began in the U.S. in 1976;14 airborne pollution from this source was the primary cause of lead intoxication, with lead from paints and from solder in food cans generating further exposures.

As documented by the National Health and Nutrition Examination Surveys (NHANES) blood lead levels in Americans aged 1–74 declined by 78% between 1978 and 1991, and by 76% in ages 1–5. 15 Subsequent research shows the aIt is stated on p.1 of City Crime Rankings11 under the heading “Methodology”: “First, city and metro crime rates for six basic crime categories—murder, rape, robbery, aggravated assault, burglary and motor vehicle theft—were plugged into a formula that measured how a particular city or metro area compared to the national average for a given crime category. The outcome of this equation was then multiplied by a weight assigned to each of the six crime categories. For this year’s award (2000), each of the six crimes was given equal weight. By weighting each crime equally, cities are compared based purely on their crime rates and how they stack up to the national average for a particular crime category. These weighted numbers then were added together for a city or metro area’s final score.”

Fluoride 2005;38(1)

Table 1. 327 Cities grouped by population, with groups bifurcated into high and low crime sub-groups

Population Group Size

Crime level subgroup

[N/2 or (N-1)/2]

High [24]

Low [24]

High [18]

Low [18]

High [22]

Low [22]

High [15]

Low [15]

High [31]

Low [31]

Average crime index

[Difference between the high & low subgroups]

183.51

42.93 [140.58] [10.26%]

120.81 268,888

-0.57 252,535 [121.38] [6.48%]

120.73 176,726

7.09 178,424 [113.64] [0.96%]

92.29 134,370

-34.56 134,213 [126.85] [0.12%]

61.35 110,713

-42.89 110,342 [104.24] [0.34%]

Fraction of population group fluoridated

[%]

41/48 [85.417]

26/37 [70.270]

25/44 [56.818]

16/30 [53.333]

34/63 [53.968]

63/105 [60.000]

Fluoridation status of population subgroups based on the fraction of the population group fluoridated

>350,000 (C) [48]

200,000– 350,000

(D) [37]

150,000– 200,000

(E) [44]

125,000– 150,000

(F) [30]

100,000– 125,000

(G) [63]

75,000– 100,000

917,401

High 63.46 85,667 [52]

(H) [105] Low -44.62 85,453

[52]

[108.08] [0.25%]

Water fluoridation and crime in America 15

 (Data- base)

[N]

Average population size

[% difference in population

size]a

832,072

Number expected to be fluoridated

20.50 20.50

12.65 12.65

12.50 12.50

8.00 8.00

16.73 16.73

31.20 31.20

Number observed to be fluoridated

23.00 18.00

15.00 10.00

16.00 9.00

12.00 4.00

18.00 16.00

34.00 29.00

Difference between observed & expected

+2.50 -2.50

+2.35 -2.65

+3.50 -3.50

+4.00 -4.00

+1.27 -0.73

+2.80 -2.20

a The % difference in population size was calculated by taking the difference in the average population between the two subgroups, dividing by the size of the smallest group, and multiplying by 100.

Fluoride 2005;38(1)

16 Seavey

Table 2. Chi-squared statistics for 327 cities grouped by population, with groups bifurcated into sub-groups by crime level and fluoridation status

Population Group Size

Expected (based on the fraction of the population group non-fluoridated) and observed numbers of non-fluoridated population subgroups

Crime level subgroup

[N/2 or (N-1)/2]

High [24]

Low [24]

High [18]

Low [18]

High [22]

Low [22]

High [15]

Low [15]

High [31]

Low [31]

75,000– 100,000 [52]

(H) [105] Low [52]

Expected (based on the fraction of the population group fluoridated) and observed numbers of fluoridated population sub- groups

(Database)

[N]

Number expected to be

fluoridated

20.50 20.50

12.65 12.65

12.50 12.50

8.00 8.00

16.73 16.73

31.20 31.20

Number observed to be fluoridated

23.00 18.00

15.00 10.00

16.00 9.00

12.00 4.00

18.00 16.00

34.00 29.00

Difference between observed & expected

+2.50† [0.3049]*

-2.50† [0.3049]*

+2.35† [0.4366]*

-2.65† [0.5551]*

+3.50† [0.9800]*

-3.50† [0.9800]*

+4.00† [2.0000]*

-4.00† [2.0000]*

+1.27† [0.0964]*

-0.73† [0.0319]*

+2.80† [0.2513]*

-2.20† [0.1551]*

Number

expected to be non-fluoridated

3.50 3.50

5.35 5.35

9.50 9.50

7.00 7.00

14.27 14.27

20.80 20.80

Number observed to be non-fluoridated

1.00 6.00

3.00 8.00

6.00 13.00

3.00 11.00

13.00 15.00

18.00 23.00

Difference between observed & expected

-2.50† [1.7857]*

2.50† [1.7857]*

-2.35† [1.0322]*

2.65† [1.3126]*

-3.50† [1.2895]*

3.50† [1.2895]*

-4.00† [2.2857]*

4.00† [2.2857]*

-1.27† [0.1130]*

0.73† [0.0373]*

-2.80† [0.3769]*

2.20† [0.2327]*

>350,000 (C) [48]

200,000– 350,000

(D) [37]

150,000– 200,000

(E) [44]

125,000– 150,000

(F) [30]

100,000– 125,000

(G) [63]

High

*(Observed- Expected) 2/Expected. Total for high crime subgroup 10.9522, low crime subgroup 10.9705, both subgroups χ2 =21.9227

†Comparing the expected and observed numbers of subgroups that were fluoridated. p<0.05, χ2=21.9227, df=11.

Fluoride 2005;38(1)

Water fluoridation and crime in America 17 continuation of this decline at a reduced rate through 1994.16 (See Figure, which plots historical data with solid lines, projects these trends with dashed lines, and compares trends for lead and crime levels, starting with peak numbers for each representing 100% on the same scale.) Lagging the peak and decline of lead levels by about 13 years, violent crime peaked in 1991, and decreased about 30% by 2000.a,17

Blood lead μg/dL 109 4000

US average crime rate per 100,000 population in children aged 1–5 yrs

8 7 3000

15 14 13 12 11

6000 5000

6 5 2000 4 3 2 1 0

0 1976 1980 1984 1988 1992 1996 2000 2004 2008

NHANES NHANES NHANES II III–1 III–2

NHANES = The National Health and Nutrition Examination Surveys Figure. Declines of blood lead and crime

RESULTS

Part A: Media-reported crime database and fluoridation

The carnage for 134 executed events in database “A” includes 325 killed and 224 wounded—about 4.1 casualties per event. b At the midpoint of the period in which these events occurred—March 1997—an estimated 57.5% of the US population was fluoridated. c Of the total of 152 executed and ideational events listed in database “A”, 128 (84.21%) occurred in fluoridated communities or were committed by criminals from fluoridated communities. Of 128 locations

A City Crime Rankings17 shows that crime had hit a similar peak of 5,850 per 100,000 in 1981, dropped to 5038.4 for unclear reasons by 1984, and then increased for 7 years to its 1991 peak of 5,898.4. bThe 1995 bombing of the Federal Building in Oklahoma City is included in database “A”, but the casualties [168 killed, 853 wounded] are not included in this summary, as they would badly skew the portrayal of a typical event. Timothy McVeigh, the convicted bomber, grew up in the fluoridated town of Pendleton, New York, and was stationed at two fluoridated army bases, Fort Benning, GA, and Fort Riley, KS. McVeigh’s remorseless lack of empathy for his victims is believed to exemplify the mental condition of a fluoride-intoxicated killer.

C Data extrapolated/projected from chart and graph, p. xxii- xxiii of Fluoridation Census 1992. US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Prevention Services, Division of Oral Health, Atlanta Georgia 30333. September, 1993. An annual increase in the fluoridated population of 0.4%, from a 12/31/92 level of 55.8%, is projected.

1000

Fluoride 2005;38(1)

18 Seavey related to these events, 98 use silicofluorides, 17 use sodium fluoride, 12 have natural fluoridation, and one combines natural and artificial fluoridation. The average fluoridation level for these 128 communities is 0.983 ppm, and the range is from 0.3 ppm to 4.9 ppm.

Using a population mean of 0.575, a one-sample t test determined the probability of randomly selecting from a 152-count simple random sample (SRS) a sample mean of 0.8421. The null hypothesis, that water fluoridation and these violent crimes vary independently and are unrelated, is rejected (P<0.0005, t=9.001, df=151).18 For database “B”, it was expected that 57.3%, or 94 of the 164 locations identified would be fluoridated. The sample mean was 98 of 164, or 59.8% (one-sample-t-test: P>0.25, t=0.5883, df=163). The chance is thus better than 1 in 4 that the null hypothesis is true, i.e., that fluoridation and gun-based self-defense are randomly associated. So this is a useful control, allowing us to rule out fluoridation-related vagaries of crime reporting or of firearm distribution as a basis for the findings in database “A”. Nevertheless the only valid inference from database “A” concerns the extreme improbability of randomly observing 84.21% fluoridation-related events in a 152-count SRS when only 57.5% were expected.

Crime reporting in the media, and the statistical categorization of crime by the F.B.I., lack at this time a nuanced awareness for identifying “fluoride-related” crime. Whether database “A” demonstrates the objective existence of such a category, or whether it demonstrates that an observer can learn to identify such events from subtle cues found in news stories, it may be seen that both possibilities strongly suggest that such a category exists. The development of database “A” was in any case a necessary step for building a hypothesis of a connection between water fluoridation and crime.

Part B: Online crime database and fluoridation

The six population groupings eliminate city size as a confounding variable, and provide a spread for analyzing variance. Each of the six High Crime subgroups had an average “score” or “crime index” at least 100 points above its corresponding Low Crime subgroup. All six High Crime subgroups had more places fluoridated than expected; all six Low Crime groups had fewer places fluoridated than expected (P<0.05, χ2 = 21.9227 df =11).19 This validates the following preliminary inference: “In American cities having population over 75,000, high crime levels appear to be significantly correlated with water fluoridation.”

Part C: Book crime database and fluoridation

The results are summarized in Table 3. The fluoridation status “Combined”— which is a combination of natural and artificial fluoridation—is an anomaly in having a crime rate 2.9% lower than the non-fluoridated cities.

All of the other types of fluoridation are associated with elevated crime rates. Compared to the crime rate for non-fluoridated cities, natural fluoridation shows a 16.5% higher crime rate; sodium silicofluoride a 37.6% higher crime rate; hydrofluorosilicic acid a 46.8% higher crime rate; and sodium fluoride an 84.9%

Fluoride 2005;38(1)

Water fluoridation and crime in America 19 higher crime rate. Table 3 incorporates population data which are used to convert these elevated crime rates into a putative number of excess crimes associated with water fluoridation in these cities.

Fluoridation statusa

No 122 fluoridation

Combined (natural 12 & artificial)

Natural 18

Sodium silico- 56 fluoride (NaSiF6)

Hydrofluorosilicic 112 acid (H2SiF6)

Sodium fluoride 7 (NaF)

Totals 327 Averages –

Table 3. 327 cities grouped by fluoridation stat

Num- Average ber population

Total population b

Total for 6 major crimes for year 2000

Crime rate, for 6 major crimes, per 100 000 population

Crime rate compared to no fluoridation cities

of cities Excess crimes compared to no fluoridation

cities c

1,813.9 1,760.8 2,112.5 +298.6 +15,322

159,099

443,526

285,077

341,713

257,890

213,962

– 242,756†

19,410,033 352,077 5,322,307 93,715 5,131,391 108,401 19,135,905 477,747 28,883,706 769,289 1,497,736 50,245

79,381,078 1,851,474 – –

0.0 -53.1 -2,826

*The data are from database “327”. aFluoridation data are generally taken from Fluoridation Census 1992 [US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Prevention Services, Division of Oral Health, Atlanta, Georgia 30333, USA; September, 1993] with some corrected and updated information based on telephone inquiries. The category “Other” identified in the Fluoridation Census 1992 has been identified here as “Combined”. bPopulation and crime data are from Morgan KO, and Morgan S, editors, City Crime Rankings, 8th ed. Lawrence, KS: Morgan Quitno Press; 2001. c“Excess Crimes” are calculated by dividing the total population figure on a line by 100,000 and multiplying the result by the crime rate compared to no fluoridation cities on that line. These “excess crimes” are only those for the 327 cities over 75,000 population, totaling 28.5% of the US population. †The total population, 79,381,078, divided by 327, yields the average population per city, 242,755.5902, which is rounded to the nearest whole number. ‡First, the total population, 79,381,078, is divided by 100,000, yielding 793.81078. Second, the total number of crimes, 1,851,474, is divided by this 793.81078, yielding the quotient 2332.387071, which is rounded to two decimal places. This is the average crime rate per 100,000 population for all the 327 cities, including the 122 which are not fluoridated.

2,496.6

2,663.4

3,354.7

– 2,332.39‡

+682.7 +130,640

+849.5 +245,367 +1,540.8 +23,077

– +411,580 – –

0.0

Fluoride 2005;38(1)

20 Seavey Part D: Lead related crime

If we accept the premise that the observed decline in crime is the result of the decline in lead intoxication, we can roughly quantify the amount of crime associated with lead intoxication by comparing the curves for the historical declines in lead and crime, and by projecting them forward from 1993 and 2000, respectively. (See Figure on page 17.)

Projecting the lead level decline on a straight line, it reaches zero by the beginning of 2004. This is an analytically useful end point, even if lead levels will more likely taper off on a curve to a steady state reflecting more or less permanent levels of environmental pollution. The crime decline is projected beyond 2000 along a straight line following its 9-year trend. Note that at the point in time where the straight-line projection for lead reaches zero, the crime rate is still at about 3,365 per 100,000, down from its 1991 peak near 5,900.a

It is thus estimated that by 2004, with blood lead reduced to minimal levels, we will still have 57% of our 1991 peak crime level. It follows that less than half of the 1991 peak level of crime can be attributed to lead intoxication. Alternatively, we would have to hypothesize that relatively low levels of lead generate disproportionately large amounts of crime, and that the relationship between lead levels and crime is extremely non-linear, to a degree that we have seen no reason to suspect.

DISCUSSION

The data show a consistent association between water fluoridation and high crime levels. The traditional socio-cultural determinants of crime—poverty, crowded cities, broken homes, drug use, gangs, and the like—have not been analyzed here as confounding factors, so a causal role for fluorides in crime has not been definitively proven, nor has the role of fluorides been quantitatively established vis-à-vis these other factors. And while conclusions about the statistical significance of findings in Part B remain tentative, all the data nevertheless point in the same disturbing direction, raising serious questions as to whether water fluoridation could possibly be as “safe and effective” as public health authorities and dentists have claimed it to be.

The information on sodium fluoride—despite the small sample—is of particular interest, since sodium fluoride, unlike the silicofluorides, shows little association with elevated blood lead levels.9 It thus appears that sodium fluoride may be associated with crime independently of lead. If sodium fluoride—a salt which dissociates into sodium and fluoride ions in water—is associated with crime independently of a role in the uptake of lead, given that sodium is a normal and well-regulated feature of the human system, it follows that the fluoride ions must be the factor associated with the crime. It then follows that, even in the case of the silicofluorides, the fluoride ions must themselves be contributing to crime

aNote that these rates include larceny and theft, in addition to the six major crimes reported on elsewhere in this paper, so the total rates are higher and cannot be compared to the aggregate rates for the six major crimes reported by MQP.

Fluoride 2005;38(1)

Water fluoridation and crime in America 21 independently of silicofluoride’s role in the uptake of lead. Bear in mind that these crime statistics are from the year 2000, when environmental lead had been significantly reduced, and that while the MQP crime data are for the year 2000, the data from the Fluoridation Census are from 1992. The latter are less recent, obviously, but they are the most recent readily available data.

Chemical exposures clearly affect brain function and behavior: lead and mercury are well documented in this regard, and fluorides are gradually becoming better understood. Chemically based crime causality, however, seems to be of a qualitatively different order from the traditionally-accepted types of socio-cultural crime causality. The relationship between these broad categories of causality needs further study, and perhaps a new paradigm is needed to integrate them into a coherent theory.

If the history of lead is any example, however, there may be reason for optimism. Unlike the seemingly intractable socio-cultural determinants, chemical exposures may be amenable to long-term change.

Crime is a measure of social dysfunction, and a barometer for socio-economic dislocation and change. Its causes are infinitely varied in their particulars, nebulous in their totality, and they vary historically from one era to the next. The historical context at any given time, moreover, cannot be duplicated experimentally, challenging the use of scientific methods; and the data that are available to us tend to be colored to some extent by the preoccupations and motives of the era and the people that produced it. There is thus an evident need for an interdisciplinary approach to crime, and for a paradigm which integrates chemistry, statistics, sociology, and history, at a minimum.

The post-Civil War era, for example, saw a significant rise in American crime rates.20 The war may have inured the population to violence; the post-war westward expansion may have created a less-well-ordered frontier society; or those frontiers may have included numerous areas with high fluoride levels in the groundwater—three competing explanations which would doubtless challenge the available data. And while the data in this study focus on the United States during the 1990’s, there are nearby anomalies such as unfluoridated Vancouver, British Columbia., which has experienced high crime rates associated with gangs, drugs, immigration, and ethnic conflict. Immigration, migration, and relocation create difficulties in tracking exposure to fluorides. In the United States, the Clean Air Act (1970) did not address airborne fluorides at all, so we have virtually no data for evaluating exposures from this source.

The senseless multiple shooting became the signature crime of the 1990’s in the United States. Fluoride exposures in many areas may have passed a threshold beyond which “fluoride-related crime” became common. Saturation of Americans with fluorides, via public water supplies, continues to expand. I think we can currently discern the resultant crime effects due to their locational variations. If water fluoridation were ended, it might take a generation for the effects to recede. If it continues to expand, the “signal” identified in this study may get lost in the “noise” of endemic violence.

Fluoride 2005;38(1)

22 Seavey

ACKNOWLEDGEMENT

The author wishes to thank Phyllis Mullenix for pointing out Grandjean’s article. I would also like to thank Prof Burgstahler for his help in organizing this material, and Dr Spittle for his patience in formatting and typesetting it.

REFERENCES

  • . 1  Grandjean P, Juel K, Jensen OM. Mortality and cancer morbidity after heavy occupational fluoride exposure. Am J Epidemiol 1985;121:57-64. 

  • . 2  Li XS, Zhi JL, Gao RO. Effect of fluoride exposure on intelligence in children. Fluoride 1995;28(4):189-192. 

  • . 3  Zhao LB, Liang GH, Zhang DN, Wu XR. Effect of a high fluoride water supply on children’s intelligence. Fluoride 1996;29(4):190-2. 

  • . 4  Xiang Q, Liang Y, Chen L, Wang C, Chen B, Chen X, et al. Effect of fluoride in drinking water on children’s intelligence. Fluoride 2003;36(2):84-94. 

  • . 5  Varner JA, Horvath WJ, Huie CW, Naslund HR, Isaacson RL. Chronic aluminum fluoride adminstration: I. Behavioral observations. Behav Neural Biol 1994;61:233-41. 

  • . 6  Varner JA, Jensen KF, Horvath W, Isaacson RL. Chronic administration of aluminum-fluoride or sodium-fluoride toratsindrinkingwater:alterationsinneuronalandcerebrovascularintegrity. Brain Res 1998;784:284-98. 

  • . 7  Mullenix PJ, Denbesten PK, Schunior A, Kernan WJ. Neurotoxicity of sodium fluoride in rats. Neurotoxicol Teratol 1995;17(2):169-77. 

  • . 8  Needleman HL, Gunnoe C, Leviton A, Reed R, Peresie H, Maher C, et.al. Deficits in psychologic and classroom performance of children with elevated dentine lead levels. N Eng J Med 1979;300: 689-95. 

  • . 9  Masters RD, Coplan MJ. Water treatment with silicofluorides and lead toxicity. Int J Environ Stud 1999; 56:435-49. 

  • . 10  Masters RD, Coplan M. A dynamic, multifactorial model of alcohol, drug abuse, and crime: linking neuroscience and behavior to toxicology. Soc Sci Information 1999; 38:591-624. 

  • . 11  Morgan KO, Morgan S, editors. City Crime Rankings. 8th ed. Lawrence, KS: Morgan Quitno Press; 2001. p. 1-5. 

  • . 12  8th Annual safest cities award. [database on the Internet]. Lawrence, KS: Morgan Quitno Press; c2001 – [cited 2001]. Originally available from: http://www.statestats.com/cit02.safe.html. This URL is no longer available. An updated version is available at Morgan Quinto Press [homepage on the Internet] from http://www.morganquinto.com/. 

  • . 13  Morgan KO, Morgan S, editors. City Crime Rankings. 8th ed. Lawrence, KS: Morgan Quitno Press; 2001. p. 214-5, 226-7, 246-7, 262-3, 294-5, 236-7. 

  • . 14  Kitman JL. The secret history of lead. The Nation. 2000 Mar 20:11-44. p. 37. 

  • . 15  Pirkle JL, Brody DJ, Gunter EW, Kramer RA, Paschal DC, Flegal KM, et. al. The decline in blood 

lead levels in the United States: the National Health and Nutrition Examination Surveys

(NHANES). JAMA 1994 July 27;272(4):284-91.

  • . 16  U.S. Department of Health and Human Services, Public Health Service, Centers for Disease

    Control and Prevention. Update: blood lead levels – United States, 1991-1994. MMWR Morb

    Mortal Wkly Rep 1997 Feb 21;46(7):141-6. 

  • . 17  Morgan KO, Morgan S, editors. City Crime Rankings. 8th ed. Lawrence, KS: Morgan Quitno

    Press; 2001. p. 394-5. 

  • . 18  Moore DS, McCabe GP. Introduction to the Practice of Statistics. 3rd ed. New York: WH Freeman;

    1999. p. 507-12, Table D, p. T-11. 

  • . 19  Moore DS, McCabe GP. Introduction to the Practice of Statistics. 3rd ed. New York: WH Freeman;

    1999. p. 624-32, Table F, p. T-20. 

  • . 20  Pearl M. The Dante club. New York: Random House; 2004. p. 376.

    Published by the International Society for Fluoride Research http://homepages.ihug.co.nz/~spittle/fluoride-journal.htm

    Editorial Office: 727 Brighton Road, Ocean View, Dunedin 9051, New Zealand 

Fluoride 2005;38(1)

MORE LINKS ON THE SAME TOPIC:  ↓ ↓

THE TOXIC METAL CONNECTION by B. Windham

Neurodegenerative Changes in Different Regions of Brain, Spinal Cord and Sciatic Nerve of Rats Treated with Sodium Fluoride

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ASSESSMENT OF GROUNDWATER QUALITY WITH SPECIAL REFERENCE TO FLUORIDE AND ITS IMPACT ON IQ OF SCHOOLCHILDREN IN SIX VILLAGES OF THE MUNDRA REGION, KACHCHH, GUJARAT, INDIA

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FLUORIDE AND CRETINISM

… The goiter prevalence was 91% and dental fluorosis 20.80%.
The average level of iodine in drinking water was
5.21 mg/l, and that of fluoride 0.88 mg/l…

ukrainian-cretin-farm-women

 

MF-Cretins-f

Image of 3 Cretins

THE RELATIONSHIP OF A LOW-IODINE AND

HIGH-FLUORIDE ENVIRONMENT TO

SUBCLINICAL CRETINISM*

IN XINJIANG (China)

by

Lin Fa-Fu, Aihaiti, Zhao Hong-Xin,

Lin Jin, Jiang Ji-Yong, Maimaiti, and Aiken.

extract:

… Xinjiang Institute for Endemic Disease Control and Research;

Office of Leading Group for Endemic Disease Control of Hetian Prefectural

Committee of the Communist Party of China; and County Health and

Epidemic Prevention Station, Yutian, Xinjiang.

   Cretinism* in iodine-deficiency areas is well known, yet the milder forms of somatic and psychomotor maldevelopment and thyroid dysfunction caused by iodine deficiency may be more difficult to detect. DeQuervain, in 1936, called this milder form “semi-cretinism,” while in 1980 Laggasse used the term “cretinoidism.” It was formally named “subclinical endemic cretinism” at a symposium on subclinical cretinism held in Xinzhou, Shanxi province in 1985.

Currently, attention is being focused on these disorders in China and abroad. The Hetian prefecture in Xinjiang has reportedly been one of the Asian areas most severely affected by iodine deficiency disorders (IDD).

During the period 1987-1989, we made a systematic survey of subclinical endemic cretinism in this district under a UNICEF aid Project.

Materials and Methods

General conditions and selection of affected areas – The entire region of Xinjiang in central Eurasia is affected by iodine deficiency. The study area, located between the southern border of Tarim basin and the northern slope of Kunlun Mountains, is arid with sandy soil and an annual precipitation less than 50 mm. The cultivated alluvial plain extends from south to north with a steepening gradient. The geographical distributions of endemic goiter and endemic fluorosis are characterized by marked vertical zones. The inhabitants are of lower socioeconomic status, with an annual mean income of about 200 yuan (RMB) per person.

Area with high fluoride and low iodine levels (Area A) – In the township Xinyuan in the lower reaches of Kliya river in the county of Yutian, north of the highway, we examined 250 schoolchildren, aged 7-14 years. The goiter prevalence was 91% and dental fluorosis 20.80%. The average level of iodine in drinking water was 5.21 mg/l, and that of fluoride 0.88 mg/l.

Area with low iodine level (area B) – In the townships of Langan and Jiayi in the alluvial plain before the mountains and to the south of the highway, we examined 256 schoolchildren, aged 7-14 years. The goiter prevalence was 82% and dental fluorosis of 16.00%. The average water iodine level was 0.96 mg/l and that of fluoride 0.34 mg/l. …

* CRETINISM is the condition wherein the child has severely stunted physical growth due to untreated congenital iodine deficiency while myxedema is a form or cutaneous and dermal edema due to increased deposition of the connective tissue components. The subcutaneous tissues are seen in hypothyroidism and Grave’s disease.

   EFFECT OF HIGH-FLUORIDE WATER

          ON INTELLIGENCE IN CHILDREN CLICK HERE ↓  ↓  ↓  ↓

 FLUORIDE LOWERS IQ

Reports of this problem are surfacing in parts of

Australia where water fluoridation has been operating for many years!

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FLUORIDE – RAT POISON & INSECTICIDES – patents & papers

The fact that sodium fluoride would control certain
types of insects has been known for many years,
but all attempts to use it and other fluorine
compounds on plants failed because
of plant injury...

ant-looking-left

fluoride-kills-us-all

title+-rat-Mozy-credit-sss

“Fluorine has played a significant role in insect control since about 1896 when
sodium fluoride and various iron fluorides were patented in England as insecticides.

   Sodium fluoride was used in the United States for cockroach control before 1900 and was introduced in 1915 for the control of poultry lice. However, the use of fluorine insecticides did not become general until the 1930´s when the disadvantages of arsenical residues on food crops became apparent and the inorganic fluorine compounds were introduced as “safer substitutes”.

Systematic investigation of organofluorine insecticides began about 1935 in the I. G. Farbenindustrie and the fluoroalcohols and fluorophosphates (phosphorofluoridates) were intensively investigated largely through the research of Schrader (1952). During World War II fluoro-DDT or “Gix” was used for the control of insects of medical importance. More recently, fluoroacetamide and analogues have been used as systemic insecticides and a large variety of other fluorinated organic compounds have shown insecticidal activity. Sulfuryl fluoride has recently been marketed as a fumigant for household and structural pests…”

Alvord and Dietz, of Grasselli Chemical Company, Cleveland, Ohio, point out certain problems with the use of soluble fluorides as insecticides (Ind. Eng. Chem. 25 (June 1933) 629-633):

“The fact that sodium fluoride would control certain types of insects had been known for many years, but all attempts to use it and other fluorine compounds on plants failed because of plant injury. Progress along the line of utilizing the fluorine compounds in this connection really began with the discovery by Roark that the relatively insoluble fluorides would not injure the foliage and would control certain insects. About the time of this discovery, the Grasselli Chemical Company began to experiment with barium fluosilicate. The development of this material was held back for several years because of plant injury following its use, and it was not until the discovery, quite by accident, that the injury was due to an unsuspected impurity and that the pure compound was in reality safe to most foliage, that rapid progress was made.”

S. Marcovitch gives some details as to how those fluoride insecticides work (Ind. Eng. Chem. 16 (1924) 1249):

“The value of sodium fluosilicate as an insecticide is due to the fact that it is both a contact and stomach poison. Shafer has determined that when a roach walks over powdered sodium fluoride a little of the powder adheres to the lower part of the body, antennae and tarsi of the feet, and dissolves in the exudations of the integument. This seems to cause some irritation and uneasiness; the insect soon begins to clean the moistened powder from the body by licking it. In doing this enough of the poison may be brought into the mouth and swallowed, to kill after a period varying in from five to ten days. Other insects, such as Mexican bean beetles, also have the habit of cleaning themselves and by putting their feet in their mouths become very easy to kill. For this reason the sodium fluosilicate is more effective against the adult beetles than the larvae, which do not have these habits.”

Because of such habits, toxicity to higher animals became of concern (Marcovitch S.: “The fluosilicates as insecticides”, Ind. Eng. Chem. 18 (June 1926) 572-573

.
The Patents:

1896

Charles Henry HIGBEE, of New York City, N.Y., Manager of Manufacturing Company: “An improved composition or material for destroying insects”, British Patent GB 8236; filed April 18, 1896; pat. May 23, 1896. (“The compounds of fluorine which I employ for the purpose of destroying insects, are certain soluble ones, viz.: sodium fluoride, ferric fluoride, the silico-fluorides of the same bases, hydro-fluo-silicic acid, and the boro-fluo-silicates”, which the inventor claims to be less toxic for humans then many of the compounds then in use for the same purpose, i.e. “arsenic, copper, phosphorus, and the like”)

1906

Karl Heinrich WOLMAN and Bernard DIAMAND, Idaweiche, Oberschlesien, Germany, assignors to Max Marschall, Nice-Cimiez, France: “Preserving composition for fibrous material”, US Patent 934,871; filed Nov. 6, 1906; granted Sept. 21, 1909  (uses “sodium fluorid” and “sodium silico-fluorid”. “We have also found that the salts of hydrofluoric acid and of silicofluoric acid both of which are weak, bactericidal acids when used in connection wioth a strong mineral acid, as above set forth, will produce good results …”)

1908

Carleton ELLIS, assignor, by mesne assignments, to Chadeloid Chemical Company, of New York, N.Y.: “Insecticide”, US Patent 1,082,507; filed March 11, 1908; pat. Dec. 30, 1913 (“The composition comprises a solution of wax in carbon bisulfid, or similar penetrating organic liquid, emulsified with an aqueous solution, considerably thickened for the purpose of emulsification, and carrying in solution a powerful insecticide such as inorganic compounds like bichlorid of mercury and ammonium fluorid, or organic compounds like ammonium formate, etc.”)

1911

Jacques WITTLIN, of Vienna, Austria-Hungary, assignor of one-half to Siegfried Schlewinger, of New York: “Antiseptic”, US Patent 1,044,840; filed Jan. 12, 1911; granted Nov. 19, 1912 (“… my present invention further contemplates the incorporation of ammonium fluorid or equivalent fluorin-containing salts or fluorin compounds in the preparation of the antiseptic, whereby the germicidal or disinfectant properties thereof are very materially increased.”)

1921

Henry Edward Percy HUTCHINGS, of Barking Essex, UK: “Improvements in or relating to rat and other vermin poisons”, British Patent GB 187,424; filed Sept. 15, 1921; pat. Oct. 26, 1922  (a bait for the purpose of rat and mouse extermination, with additions of either sodium fluoride, barium carbonate, squill or oxalic acid, to serve as a basic poison)

1923

Rurik C. ROARK, Baltimore, Md.: “Insecticide”, US Patent 1,524,884; filed Aug. 6, 1923; granted Feb. 3, 1925 (“The poisonous action of soluble fluorides is well known and has been utilized for the control of injurious insects. For example, sodium fluoride, a salt readily soluble in water, is a very effective roach poison and is a common ingredient of roach powders. Potassium and barium fluorides have been similarly employed …”)

“There is nothing new in the use of sodium fluosilicate as an insecticide. Its use for that purpose was described nearly thirty years ago by HIGBEE (English Patent No. 8236, May 23, 1896). More recently, WILLE has reported tests with sodium fluosilicate against roaches and COBENZL mentions it as a common ingredient of rat and insect poisons” (Roark C., Department of Agriculture: “Fluorides vs. fluosilicates as insecticides”, Science 63 (April 23, 1926) 431-2)

1926

Bernard GEHAUF and Harold W. WALKER, of Edgewood, Md.: “Method of making silicofluorides and products thereof”, US Patent 1,617,708; filed May 14, 1926; pat. Feb. 15,1927 (“This invention … also comprises a new composition of matter for insecticidal and other purposes … made by neutralizing hydrofluosilicic acid with the appropriate base … Hydrofluosilicic acid ordinarily is prepared by contacting various waste gases containing silicon fluorid with water.. Waste gases containing silicon fluorid arise in various industries, as in the manufacture of superphosphates.”)

Martin J. FORSELL, Seattle, Washington: “Insecticide”, US Patent 1,618,702; filed Aug. 30, 1926; granted Feb. 22, 1927 (“The insecticide consists of using apple after it is dried and powdered and mixing therewith any well-known poison in powdered form … any one of the compounds of fluorine preferably sodium or potassium fluoride or sodium or potassium silico fluoride …)

Howard S. McQUAID, Cleveland, Ohio, assignor to The Grasselli Chemical Company, of Cleveland, Ohio: “Production of Barium Silicofluoride”; US Patent 1,648,143; filed Nov. 22, 1926; patented Nov. 8, 1927 (Process for production of barium silicofluoride from sodium silicofluoride for use as an insecticide)

1927

Hermann STÖTTER, Leverkusen, assignor to I.G. Farbenindustrie Akt.-Ges., Frankfurt a. M.: “Verfahren zum Schützen von Wolle, Pelzwerk u. dgl. gegen Mottenfraß”, German Patent (DE) 485,101; filed May 26, 1927; granted Oct. 10, 1929  (ammonium bifluoride, potassium ammonium fluoride)

1929

Roscoe H. CARTER, Washington D.C. (Government employee): “Process for the manufacture of insecticides and method of making same”, US Patent 1,842,443; filed Nov. 15, 1929; granted Jan. 26, 1932  (“As pointed out in other patent applications of mine, the double fluorides of the alkali metals are useful insecticidal materials and can be formed from water soluble salts of aluminum by treatment with alkali metal compounds and fluorine acids in the proper molecular proportions.”)

1931

Arthur H. HENNINGER, assignor to General Chemical Company, New York: “Process of making potassium aluminum fluoride”, US Patent 1,937,956; filed June 18, 1931; pat. Dec. 5, 1933 (“… for use as an insecticide. It has heretofore been proposed to use potassium aluminum fluoride as an insecticide for the control of various insect pests. This material is considered to possess advantages over lead arsenate as an insecticide for the reason that, although poisonous, the fluoride compound is less toxic to human beings and animals than is lead arsenate.”)

1932

Earl B. ALVORD, assignor to Grasselli Chemical Company, Cleveland, Ohio: “Noncorrosive insecticdal compositions”, US Patent 1,931,367; filed Aug. 24, 1932; patented Oct. 17, 1933 (addition to their barium fluosilicate of a slightly water-soluble substantially neutral fluoride (such as cryolite, or barium fluoride) to overcome corrosive effects of the barium fluosilicate upon spray pumps)

1938

John E. MORROW, assignor to Aluminum Company of America: “Insecticide and method of producing same”, US Patent 2,210,594; filed Jan. 6, 1938; pat. Aug. 6, 1940 (“Double fluorides of sodium and aluminum, such as natural and synthetic cryolite, have been used as insecticides, and the usefulness of such compounds as stomach poisons for various insects has been established. It has been demonstrated, for example, that these fluorides are particularly useful in combatting the codling moth and the Mexican bean beetle.”)

1948

Alan BELL, Kingsport, Tennessee, assignor to Eastman Kodak Company, Rochester, N. Y.: “Insecticidal compositions comprising either hexyl alkyl tetraphosphate or tetra-alkyl pyrophosphate and either an alkali metal fluoride or fluorosilicate”, US Patent 2,514,621; filed Dec. 26, 1948; granted July 11, 1950  (“Diethyl phosphate is the hydrolysis product produced by most of these phosphorus insecticides such as organic insecticides derived from triethyl phosphate – thionyl chloride reaction product, hexaethyltetraphosphate, tetraethylpyrophosphate. This hydrolysis product is not as toxic as parent compound in itself but mixed with NaF or Na2SiF6 has considerable toxicity.”)

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Lab Rat

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fluorine-toxicosis

Rats Research – Fluoride 1934

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    One Tube of Toothpaste – Cheap 3 Months Rat & Mouse Free

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Extract: The Complete Dinosaur’ + info from China

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‘DEATH IN THE AIR’ – George Glasser +

For the phosphate fertilizer industry, water fluoridation is
an efficient, cost-effective solution for dumping pollution.

An Outbreak of Industrial Fluorosis in Cattle

f.-as-air-pollutants

CORRODED-STRIP

Polonium 210

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 See by the same author  → FLUORIDE THE PHOSPHATE CONNECTION

Artie Johnson is a young African American woman, the mother of three children.
She worked for Occidental in the superphosphoric acid evaporation plant at the Swift Creek Chemical Complex for almost nine-years. She is a plaintiff in the toxic tort lawsuit, but she is unable to speak for herself because of chemical induced neurotoxic damage form working at Occidental Chemical Corporation. Artie and her three children live with her mother, Eartha Coffee, who works, raises the children and tends to Artie’s needs.

Artie is an enigma. Gary Pittman who was her supervisor speaks highly of her as an intelligent young woman, good person and excellent employee. As Pittman puts it, “Artie was like one of the boys, and a better employee than many. She worked hard and seldom complained. I was impressed with her from the first day she came to work.” Gary speaks of Artie in the past tense, because she is not the same bright, charming person he once knew.

One can only imagine the poignancy of her story, because she suffers with Alzheimer’s disease-like memory loss and confusion among other health problems. Today, Artie Johnson basically exists in a void while most women are watching their children grow-up, or have some sort of life. It would seem that even a life of hardship would be better than that of utter confusion and not remembering who you are at times.

It is most commendable that the plaintiffs in the toxic tort lawsuit chose to include Artie Johnson and become a collective voice for someone who can no longer speak for herself as with the two deceased plaintiffs, Bobby Hobby and Roy Mathis.

Gary Pittman, Clinton Vann, Jesse Nash, Billy Baldwin, Bobby Brown, their wives and families have stepped forth to speak for those who are afraid, and those who can no longer speak for themselves: Artie Johnson represents those people in the toxic tort lawsuit against Occidental Chemical Corporation.

Section 15(a) of the complaint filed against Occidental Chemical Corporation best sums-up the attitude of elite Occidental management toward employees at the chemical complexes: “The Defendants knew that toxic substances were present in virtually every area of the plant, except for the area which was occupied by management personnel, which was seven miles from the areas and complexes where workers such where Plaintiffs would work.”

Prologue

George Glasser

In beginning this story, I thought about the format. Having read many journalistic endeavors on various subjects, I always found it difficult to maintain interest because of the dry objective style. Reviewing the accounts of the workers, wives and families, I felt that each individual had a story. I was communicating with the experts, the people who had been through good times and bad times. The technical aspects were well covered by the workers; I was an outsider looking in. It would have been presumptuous and arrogant to play the role of the objective journalist. Consequently, I thought it best to compile and edit the individual accounts. They are living the stories and I am not.

The accounts I read were home spun and rough edged, but they came from the heart. Work histories and depositions were intensely professional, and the workers insisted that technical details be correct down to whether a pipe diameter was 18 or 24 inches. The wives of the men exhibited courage and compassion. Wives of the men who are still alive oddly spoke of their husbands in the past tense.

Artie Johnson’s mother even speaks of her daughter in the past tense. Everyone who worked with Artie spoke kindly about the young mother of three children. Artie suffers with toxic brain syndrome and cannot speak for herself.

When Gary Pittman called, I thought he was another person wanting advice. However, Gary was different; he was gritty and down to earth. We shared a few chemical accident stories and got down to business. I liked Gary right off the bat. Gary didn’t want advice. Gary called to thank me for writing an article about the phosphate industry. Gary and his friends were suffering from chemical poisoning. They had worked for Occidental Chemical Corporation in Hamilton County, Florida. Now they were disabled, out of work and looking for answers. Two people in the group had died of cancers and the rest were suffering from debilitating health conditions.

Living on the edge of the Bone Valley phosphate region of West Central Florida, I knew much of what Gary was talking about, but I had never heard the real story from an inside source. I had always depended on bits and pieces of information extracted from studies, books and articles about the phosphate fertilizer industry. People who worked in the industry were reluctant to offer information about the inner workings. Phosphate fertilizer corporations rule the roost in Florida. Most employees are loyal to the companies because they offer good wages in primarily rural, agricultural communities where the only other options are picking tomatoes or working at the convenience store.

Florida phosphate mines produce 30% of the world supply and 75% of the U.S. supply of phosphate fertilizers, upwards of 20-30 million tons per year. Much of the nation’s supply of fluorosilicic acid used as a water fluoridation agent is also produced in Florida from pollution scrubbing operations. Phosphate fertilizer suppliers have more than $10 billion invested in production facilities and mining operations in Florida alone. In Florida, phosphate fertilizer production accounts for $300 million in wages, directly employs about 8,000 people and supporting industries employ an estimated 50,000 people.

In spite of this impressive resume, for many of us living in the phosphate producing regions of Florida, Saddam Hussein would be regarded as a better neighbor than the phosphate fertilizer industry.

Phosphate fertilizer is made from phosphoric acid. The chemical complexes produce phosphoric acid by mixing sulfuric acid with finely ground phosphate ore slurry. The process releases primarily, highly toxic silicon tetra fluoride vapors laced with heavy metals, radionuclides, sulfur dioxide, etc. The complexes also produce the sulfuric acid creating highly toxic sulfur dioxide gas.

All the public relations firms they hire and all the politicians they buy do not change the dirty reality of the business. Much of the phosphate producing regions of Florida are toxic waste dumps for phosphate fertilizer manufacturers. In West Central Florida, the sixty by thirty mile strip ends at Tampa Bay is called “the hot zone” by people who are environmentally aware.

For people living in these “hot zones,” the incidence of osteoblastic leukemia and lung cancer is twice the state average. As a state, Florida has a higher per-capita incidence of cancer than most states.

For every 1400 tons of phosphoric acid, 7,000 tons of waste gypsum is produced leaving barren, radioactive mountains of acidic phosphogyspum wastes. These gypsum stacks are contaminated with toxic fluorides, radionuclides, heavy metals, and sulphates. The stacks will stand for millennia as toxic monuments to the phosphate fertilizer industry.

A sinkhole, 100 feet in diameter and three or four hundred feet deep dumped millions of tons of radioactive, phosphogyspum wastes into the Central Florida aquifer.

One spill in 1997 from a settling pond atop a gypsum stack killed most of the fish in the Alifia River, outside of Tampa, Florida.

Toxic wastewater evaporates in the searing Florida sun. Hydrogen fluoride is released with other contaminants. According to an article in the Florida Scientist, 1987, by Dr. Howard Moore (deceased), a series of reactions takes place between suspended solids and hydrogen fluoride in the presence of moisture. The reactions create pollutants that can be carried far from the ponds on air currents (possibly hundreds of miles from the site). A company in Manatee County, Florida had so contaminated the air, they had to buy the air rights around the facility.

Abandoned strip mines filled with murky, lime green radioactive water dots the phosphate producing regions of Florida.

Lifeless evaporation ponds holding up to 500 million gallons of toxic, radioactive waste water surround production facilities. In one year, more than one billion gallons of the toxic wastewater spilled into Florida water ways.

Developers build homes on reclaimed mines, or the land is pasture for cattle to graze. Ambient radon levels are very high.

The radioactive phosphogyspum waste has been used to make road beds.

Runoffs from the operations contaminate the waterways and the bays of Florida.

Dusts consisting of radionuclides, sulphates and fluorides contaminate the air surrounding the phosphate fertilizer chemical complexes.

Radium wastes from the filtration systems are among the most radioactive types of NORM wastes (naturally occurring radioactive material). The radium wastes are so concentrated, they cannot be disposed of at the one landfill in the United States licensed to accept NORM wastes. The federal government has no rules for its disposal: The manufacturers bury the radioactive wastes in the gypsum stacks.

All of the above poses significant sources of potentially carcinogenic radioactive and fluorine pollution. Yet, Florida has neglected to establish laws governing the pollution generated from these sources except requiring liners for new gypsum stacks. The USEPA is reluctant to act, and nothing is being done to protect people or the environment from the pollution.

The phosphate fertilizer is basically exempt from federal regulations.
In 1980, the U.S. Congress passed Solid Wastes Disposal Act Amendments (commonly called the Bevill Amendment) to the Resource Conservation and Recovery Act. The Bevill Amendment exempted certain wastes, byproduct phosphogyspum and waste water from the wet process phosphoric acid production.

Basically, all the companies have to do with the toxic, acidic waste water is adjust the pH to 7.0 and they can dump the toxic water into the rivers and bays.

Before 1970, pollution from phosphate fertilizer manufacture was a major environmental problem in West Central Florida: May 14, 1970, Death of A Bay, St. Petersburg Independent: “BRADENTON– The specialists agreed yesterday – Bishop Harbor’s illness is terminal . . . The fluorides are the final executioners for harbor life. For once the plant life is gone, with it goes the breeding grounds for new generations of marine life. And Bishop Harbor was a nursery for marine life, a mother for Tampa Bay’s fish.”

During the late 1960′s, fluorine emissions were damaging crops, killing tropical fish, destroying the environment and causing crippling skeletal fluorosis in livestock. USEPA became concerned and enforced regulations requiring manufacturers to install pollution scrubbers. At that time, the facilities were dumping the concentrated, acidic pollution directly into waterways leading into the waterways and stacks were belching highly acidic, slightly radioactive pollution into the atmosphere.

While reading this, a person may think that the problem is regional and does not pertain to anyone living outside the phosphate producing regions of Florida. However, that is not the case. In the late 1960′s, Ervin Bellack, USEPA chemist and a manufacturing representative put their heads together and worked out the ideal solution to a monumental pollution problem. The recovered phosphate fertilizer manufacturing pollution contained about 19% fluorine. The concentrated pollution “scrubber liquor” was perfect to use as a water fluoridation agent. It was a liquid and easily soluble in water unlike sodium fluoride (the waste product from aluminum manufacturers). It was also inexpensive, and there was a glut of the concentrated toxic waste.

Fate also intervened. The aluminum industry who previously supplied sodium fluoride for water fluoridation was facing a shortage of fluorspar used in smelting aluminum. They began to recover fluorine and make synthetic fluorspar.
Consequently, there was a shortage of sodium fluoride to fluoridate drinking water. Ervin Bellack and the industry seized the opportunity to fill the gap in the market and dump the new source of recovered pollution into America’s drinking water.

For the phosphate fertilizer industry, the shortage of sodium fluoride was the key to turning red ink into black and an environmental liability into a perceived asset. The concentrated pollution could be dispersed into drinking water throughout the United States, one drop at a time. With the help of the USEPA and Ervin Bellack, fluorosilicic acid was not regarded as concentrated toxic waste anymore, a liability. It became “FLUORIDE, the proven cavity fighter.”

USEPA and U.S. Public Health Service waived all testing procedures and expedited the disposal of the radioactive concentrate into America’s drinking water as “New and Improved FLUORIDE.”

Immediately, without any oversight, clinical or safety studies, the U.S. Public Health Service and American Dental Association encouraged cities to use the pollution concentrate for drinking water fluoridation.

1976, the Resource Conservation and Recovery Act (RCRA) opened the door for USEPA to work with industry and actively find markets for recovered pollutants such as fluorosilicic acid.

By 1983 the official USEPA policy was: “In regard to the use of fluosilicic (fluorosilicic) acid as a source of fluoride for fluoridation, this agency regards such use as an ideal environmental solution to a long-standing problem. By recovering by-product fluosilicic acid from fertilizer manufacturing, water and air pollution are minimized, and water utilities have a lowcost source of fluoride available to the communities.” (Rebecca Hanmer, Deputy Administrator, Office of Water, USEPA, 1983 correspondence to Dr. Leslie Russell stated USEPA position on water fluoridation).

In promoting the use of the pollution concentrate as a fluoridation agent, the ADA, Federal agencies and manufacturers failed to mention that it was hot, radioactive. Uranium and all of its decay rate products are found in the raw phosphate rock, fluorosilicic acid and in the phosphate fertilizer. Before 1991, upwards to 75% of the U.S. supply of uranium oxide to fuel the nuclear industry was produced in Central Florida. However, today, uranium is not extracted because of economic reasons.

During the wet process manufacturing trace amounts of uranium and its decay rate products are released and captured in the pollution scrubber. As long as the amount of contaminants added to the drinking water (including radionuclides in fluorosilicic acid) do not exceed the limits set forth in the Safe Drinking Water Act, the EPA has no regulatory problem with the use of any contaminated products for drinking water treatment.

While uranium and radium found in fluorosilicic acid are known carcinogens, two decay rate products of uranium are even more dangerous and carcinogenic: Radon-222 and Polonium-210.

During the acidulation process that creates phosphoric acid, radon (a gas) contained in the phosphate pebble can be released in greater proportions than other decay rate products (radionuclides) and carried over into the fluorosilicic acid. Polonium may also be captured in greater quantities during scrubbing operations because like radon it is easily soluble in acid and can readily combine with fluoride.

USEPA is responsible for regulating radionuclide levels in the air and drinking water; consequently, they are aware that Radon-222 decays into Lead-210 in 3.86 days. The lead isotope does not give off harmful alpha radiation for twenty years until it turns into Polonium-210 (beta radiation is also harmful). Unless someone knew to look for specific isotopes, no one would know that a transmutation to the extremely radioactive Polonium-210 occurs.

Polonium-210 may be the most insidious and most significant health threat in the pollution concentrate. Polonium gives off intense alpha radiation for 138 days until it turns into regular lead and becomes stable. During the 138-day period, a very small amount can be very dangerous.

The lead-210 isotope behaves like calcium in the body. It may lay stored in the bone or body tissues for up to twenty years before it explodes like a carcinogenic, time released nuclear devices as polonium-210.

The fluoridated water someone drinks today, may be the cause of cancer twenty years down the road. No one knows what the consequences of using the pollution concentrate because there has never been any clinical research done with the product.

One particle of polonium-210 gives off 5,000 times more alpha radiation than the same amount of radium. Damage occurs in the body from complete tissue absorption of the energy of the alpha particle. Scientists say that polonium-210 can be carcinogenic to people if exposed to more than 0.03 microcuries (6.8 trillionths of a gram).

Scientists write 6.8 trillionths of a gram as 6.8 x10-12g because it would appear as 0.0000000000068 grams. Figures like that are hard to grasp to the average person, but they show that polonium is harmful to humans in very minute amounts.

Use of the pollution concentrate to fluoridate drinking water places one at risk continuously. Drinking water fluoridated with fluorosilicic acid contains radon at every sequence of its decay to polonium. Also, the fresher the batch of pollution concentrate, the more polonium it will contain. The more water fluoridated with the pollution concentrate someone consumes, the better the chances of developing cancer. It all boils down to the luck of the draw. It all depends on how much is stored in the body and in what tissue.

Not only does the fluorosilicic acid contain the contaminants inherent to the phosphate rock/pebble, but additives used during production. The pollution scrubbers are not selective with regards to washing the fumes. The quality of the product also depends on whether recycled evaporation pond water is used. Sludge from sulfuric and phosphoric acid production are dumped into the evaporation ponds atop the gypsum stacks. The radioactive scale is buried there. If a thirsty bird or raccoon ventures to the evaporation pond out of thirst, it is their last drink.

There are many factors involved in the creation of the fluorosilicic acid that are very alarming. It contains many other chemicals, organic and inorganic. During the concentration process, these chemicals are boiled off the acid in a partial vacuum at very high temperatures, equal to about 500 degrees F. The chemicals used are oil-based defoamers (possibly containing dioxins), polymers, petroleum products, naphthalene, chlorides, sulfides and various reagents. The vapors from all these chemicals are washed and captured in the pollution scrubbers along with the fluorine and fluorosilicate gases. Although it is more convenient for scientists to believe the pollution scrubbing is discriminate, it is not. One scrubber catches all, including pollution from tank farms and other processes.

About 6.8 milligrams of 23% fluorosilicic acid is added to the drinking water to achieve fluoridation at one part per million. The fluorosilicic acid is only the primary ingredient in a complex, highly toxic product. Because of the nature of creating the product, complex interactions have to occur during manufacture, e.g., heat, negative atmospheric pressure, catalyzing effects due to contact with metal vessels and additives. Of the 6.8 milligrams of product, 5.8 milligrams is contaminant laden water.

Today, 50% of all communities (about 100,000,000 people) in the United States fluoridating drinking water are exposed to the same toxic pollution that has cause so many health and environmental problems in Florida. After reading the following series of stories about the workers and their wives, one has to wonder about the sanity of using captured pollution to fluoridate drinking water.

Introduction

‘DEATH IN THE AIR’

George Glasser

In the early predawn hours when the air is still and moist, phosphate fertilizer factories are often shrouded in an acidic haze. Temperature inversions form airy bubbles of noxious, acidic fumes. Lights from the factories seem to blaze through the hellish mist, and the lemony taste of sulfuric and hydrofluoric acid leaves the lips tingling with a slight burning sensation. Then the delicate tissues in the nostrils begin to tingle with a stinging sensation. Floating and sparkling in the still morning air, microscopic, acid droplets splash against the thin film of fluid protecting the eyes and subsequent burning and watering blur one’s vision. And finally, the full impact of inhaling the noxious smog causes choking and coughing. Sometimes, the misting hydrofluoric, fluorosilicic, phosphoric and sulfuric acids are so concentrated, they actually etch the windshields and eat the paint of cars passing through the acidic fog.

For those employed at the phosphoric acid factories, this is the work world they enter every day. Day-in and day-out, they eat, breath, and drink toxic pollution until they become too sick to work, or die.

Gary Owen Pittman was one of those people. While Gary and his coworkers worked midst the toxic, corrosive fumes, the corporate elite at Occidental Chemical Corporation sat safely in well-ventilated, air-conditioned offices some seven miles from the factory.

The emissions were so acidic at the plant, visiting secretaries complained of their panty hose being dissolved while on their legs. Reassuringly, management said they had come into contact with some chemicals, but there was nothing to worry about.

Gary’s first and last job was working for the Occidental Chemical Corporation phosphoric acid factories in Hamilton County, Florida. Gary Pittman was eighteen years-old and in excellent health when he started to work as a sample man in the analytical laboratory of the Occidental Chemical Corporation, Suwannee River Plant. He rose from a $4,000 sample man in the laboratory to supervising one third of Occidental’s Swift Creek plant, earning about $50,000 a year.

Today, Gary is unable to work and suffers from auto immune disorders, toxic myopathy, chronic obstructive lung diseases with emphysema, chronic bronchitis, blood disorders, chronic fatigue syndrome, liver dysfunctions, polyarthritis, swelling of feet and lower legs, muscle weakness, cardiac arrhythmia, reactive depression, and memory loss. He walks with waddling gate and suffers dizziness: the diagnosis is toxic brain syndrome.

Gary is afraid to take his children to Disney World. He becomes too fatigued, his lower legs and feet begin to swell from walking, and may suffer an episode of cardiac arrhythmia. Emergency room records show repeated visits for irregular heart beat problems.

Gary Pittman does little these days except surf the Internet to learn more about the toxic effects of chemicals to which he and his coworkers were exposed. The list reads like the top forty toxic chemicals on Superfund Priority List of hazardous substances that pose the most significant threat to human health. The chemical exposures left him unable to work at the age of 39, and five years later, Gary Pittman finds difficulty in enjoying the simple pleasures of life.

The adverse environmental and health effects from phosphoric acid production are well documented in newspaper articles from the 1970′s, 80′s and into the 1990′s. But to the author’s knowledge, the USEPA and Centers for Disease Control (USCDC) have never commissioned any substantive studies.

USEPA New Source Performance Standards (NSPS) state: “The standard sets forth limits for total fluorides, the primary pollutant of concern, 40 C.FR., pgs. 60.200-60.204.” This issue is discussed in Phosphoric Acid Waste Dialogue, Report on Phosphoric Wastes Dialogue Committee, Activities and Recommendations, September 1995; Southeast Negotiation Network.

The insidious problem with airborne fluorides are that they can be very reactive when they come in contact with moisture. When inhaled, many fluoride salts react with water (moist lung tissue) and break down into hydrofluoric acid and the component. The hydrofluoric acid with the moist lung surface, burns a tiny hole in the tissue, and the toxic component is left at the site of damage. It is like rubbing dirt into a wound or injecting a poison. The airborne fluoride salt can act to enhance the effect of the toxicant component.

Dr. Phyllis Mullenix, pioneer researchers on the neurotoxic effects of fluorides, said when toxic fluoride compounds are inhaled, it is like giving them (fluoride compounds) “running shoes.” They enter the system uninhibited and can do more damage.

People living near phosphate fertilizer plants are twice as likely to develop lung cancer and osteoblastic leukemia. While high cancer rates for people living near phosphoric acid plants are noted in magazine and newspaper articles, little is ever said about workers and their families. If health problems are evident in people living near the phosphate plants, it is only logical that employees would be at a higher risk. The people who work at phosphoric acid plants are at ground zero. Workers have to go into acid reaction chambers filled with toxic fumes and scour scale from filters and walls.

The scale is so radioactive, up to 100,000 picocuries of radium per gram, that the only landfill in the country that accepts naturally occurring radioactive wastes will not accept the scale from phosphate fertilizer production. The radioactive wastes are either buried in the gypsum stacks or dumped into holding ponds.

Crystallized, radioactive silica tetra fluoride has to be chipped from pollution scrubbers. The residual is so hard that jack hammers must be used to remove the buildup. Workers are required to go into these hell holes and perform these dirty tasks, often without adequate safety equipment. Workers are not only exposed to the naturally occurring toxic substances, but also manmade chemicals used as reagents, defoamers (possibly containing dioxins) and flocculants to more efficiently produce phosphoric acid.

The fluorosilicic acid produced in pollution scrubbers is sold as a water fluoridation agent. More than 50% of U.S. cities which fluoridate drinking water use some form of the highly toxic pollution. Neither the USEPA nor U.S. Public Health Service can produce one safety or clinical study using the highly toxic pollution.

Sulfuric acid is also essential to phosphoric acid production. The plants produce their own sulfuric acid. The acid is mixed with finally ground phosphate rock producing noxious vapors containing heavy metals, sulfates, fluorosilicates, hydrogen fluoride and other contaminants. Uncontrolled releases of highly toxic hydrogen sulfide gas are commonplace, especially during unloading in the molten state.

Sulfur dioxide and trioxide are highly toxic. Flocks of birds flying into the clouds of sulfur dioxide emissions died in mid flight and fell to the earth over the Occidental’s sulfuric acid plants, according to accounts of interviewed workers. Current books on industrial toxicology link sulfur oxides as possible carcinogens or cocarcinogens. They cause respiratory problems, heart problems, etc.

Only recently has the Florida Department of Environmental Protection (FDEP) required companies to place vinyl liners under phosphor-gypsum stacks. Because of airborne fluorine pollution, manufactures were forced by USEPA to install pollution scrubbers in the late 1960′s and early 1970′s. But, in Florida, it is common knowledge that the phosphate companies set the environmental ground rules, and the USEPA and FDEP tends to turn a blind eye regarding the violation of environmental regulations.

There is speculation that preferred treatment for phosphate fertilizer manufacturers started when the first atomic bombs were being developed. It was discovered that uranium-238 could be extracted from phosphate rock. During the post WW-II and Cold War eras, 75% of the uranium oxide used to produce nuclear weapons and fuel for the nuclear power industry came from several Florida phosphate fertilizer plants. Today, the laxity on the part of EPA in enforcing federal regulations is probably a leftover attitude from the days when phosphate fertilizer plants were a national security asset.

Although Occidental had to be aware of risks to employees, even in the mid-1960′s chemicals and contaminants associated with phosphoric and sulfuric acid production, the corporation chose to ignore the risks. During the 1980′s, OSHA and environmental laws were much stricter; however, Occidental became a contractor to supply the Soviet Union with phosphoric acid as part of the Armand Hammer trade agreement. It appears, that in order for Occidental to meet production requirements, federal regulatory agencies may have been lax in enforcing safety and environmental regulations.

Gary Pittman’s deposition for a lawsuit reads like a twenty-year sentence to hell. “When I first started working for Occidental, safety considerations were basically nonexistent. The only things we were required to wear were safety glasses. Gloves, respirators and dust masks were not furnished.

“I remember one incident when I was assigned the task of cleaning the filter hood and the pollution scrubber. Powdery fluorosilicate dust was everywhere. As we were cleaning, the fluorosilicate dust covered us, and it was very hot; we were sweating profusely. When the fluorosilicate dust mixed with the perspiration, it would form fluorosilicic acid on the skin and blister us if we did not wash it off.

“I remember going home after one episode in the pollution scrubber. I started coughing and choking. My eyes started to burn. I realized that my clothes were fuming. I rolled the window down in my truck so I could see to drive home. Reaching home, I removed my clothes and gave them to my wife to wash. Well, the only things that came out of the washing machine intact were the zipper and a couple of buttons.”

“It was common to develop acid sores, rashes and blisters after those jobs. It was also common to cough up blood after breathing the fluorosilicates and other fumes.”

Silicon tetra fluoride is a highly toxic fluoride compound. The autopsy on a man who died of several minutes exposure to concentrated fumes at a phosphate fertilizer plant revealed a coating of silica on the lungs. The cause of death, however, was determined to be fluorine poisoning. The fluorosilicates found in the pollution scrubbers contain heavy metals, radionuclides (including radium-226, radon-222 and uranium-238).

Gary also suffers with emphysema and has described classic symptoms of silicosis. In the phosphate industry, the older workers refer to the condition as “chemical pneumonia.”

Where employees are exposed to toxic substances, most manufacturers require employees to take urine tests for levels of chemical exposure. This is basic risk management procedure to protect the company against future lawsuits. In the twenty years working for Occidental, Gary had never taken a urine test, even when he became ill.

In 1987, according to Gary, Occidental management decided to shut down a pollution scrubber stating that it was not needed. For almost three years, in spite of violating state regulations and in felony violation of the Clean Air Act, Occidental operated the facility with the pollution scrubber shut down to save money. The entire population of Hamilton County, Florida was exposed to toxic emissions from the plant, possible many times what is considered safe levels. However, workers were exposed to higher levels than the average citizen.

In another incident, Occidental was fined for releasing ten times the safe levels of fluorides into the atmosphere. Over the years Gary worked for Occidental, he said that the company had been cited numerous times for OSHA and environmental violations.

By 1993, after almost twenty-one years of exposure to workplace toxicants, Gary was totally incapacitated. Suffering from degenerative muscle disease (toxic myopathy), heart arrhythmias, and emphysema, he was unable to walk up a flight of stairs and was replaced by Occidental management. He was never allowed the opportunity to try and return to work or offered another less taxing position.

None of the doctors treating Gary ever considered chemical exposure which included: Carbon tetrachloride, barium chlorides, hydrogen fluoride, fluorosilicates, sulfates, potassium cyanide, chemical solvents and many other damaging and carcinogenic chemicals. Early diagnoses included degenerative muscle disease, possible AIDS, Lyme disease, and non specific myopathy (meaning they did not know what was causing his problems).

Gary’s work history is littered with health problems and misdiagnoses by doctors who knew nothing about industrial exposure to toxic chemicals. With his numerous emergency room visits, the personnel should have put two and two together and called for toxicological testing. However, the tests were not done, not even a simple urine test. Gary’s medical profile is such that he should have been referred to an industrial toxicologist by competent emergency room personnel and doctors.

As documented in his medical and work records, with each episode of illness, Gary would take off from work and his health would improve, but after returning to work, the symptoms would return. That scenario is a text book example and typical of someone suffering from poisoning due to exposure to work place toxicants, especially fluorine poisoning.

Over the years, and despite numerous visits to doctors, Gary was never tested for industrial toxicants until he visited the Environmental Health Center in Dallas, Texas. Previously, his condition was attributed to non specific myopathy by doctors. However, Dr. Rea, the attending physician at the Dallas Environmental Health Center diagnosed Gary as having toxic brain syndrome from his previous medical records. Dr. Hickey, at the Dallas facility ran a brain spectrograph and discovered neurological damage from exposure to neurotoxins and heavy metals confirming the “toxic brain syndrome” diagnosis. Dr. Rea recommended several sessions of chelation therapy. For most people it would only take one session, but because of Gary’s poor health, normal therapy would have proven lethal, and he was unable to undergo treatment.

Numerous employees of Occidental suffer from similar medical problems including two other plaintiffs named in the lawsuit. According to Gary, employees who worked in the processing plants at Occidental “seemed to stay sick all the time. It was like they had a cold or the flu all the time. They were always taking over-the-counter medications so they could keep working.” He names numerous people with heart arrhythmias and symptoms of toxic brain syndrome. Gary also mentioned cases of Occidental employees who developed stomach cancer, lung cancer, leukemia, brain cancers, benign brain tumors and bone cancer. Several of the people with brain cancers have died.

Aside from exposure to air pollutants, the employees were also exposed to contaminants in the drinking water at the facility. Gary felt that toxic wastewater from the ponds was leaching into the aquifer. Fluoride levels in the water were between 15-17 parts per million. These levels are four times the maximum allowable contaminant level for drinking water established by USEPA. Phosphoric acid levels in the water were also very high. The drinking water was so laden with corrosive chemicals, it caused the metal pipes to crumble and be eaten away, Gary related.

Shortly before Gary was disabled, the water had become so contaminated that employees complained that it was undrinkable. A reverse osmosis system was installed. Due to the amount of contaminants, there were problems with clogging and the system was rendered ineffective. Gary requested that the company buy bottled water for the employees, but his request was denied. Rather than drink the foul tasting, toxic well water, many of the employees brought their own water to work or drank soft drinks.

In the complaint written by Gary Pittman’s attorneys, they allege that Occidental failed to provide and/or destroyed product data safety sheets and warning labels on toxic chemicals to avoid the expense of purchasing adequate safety equipment.

In documents and tapes provided by Pittman, he states that ventilation in the work areas was also poor and the equipment often failed. At one time the air-conditioning in laboratories recirculated the toxic air. During analytical procedures, toxic gases were recirculated in the rooms. “We poured all sorts of chemicals down an open drain in the floor. Sometimes they would start boiling and fuming. All those noxious fumes were recirculated by the air-conditioning system. We were continuously breathing that stuff, back then. We didn’t know any better.”

The complaint submitted by Jacksonville law firms, Coker, Myres, Schickel, Sorenson and Higgenbottom and Boyer, Tanzler and Boyer state, “Not only did the Defendants fail to provide adequate and operational ventilation, but also, to further reduce costs, the Defendants, even on occasion when the toxic fume stacks were fully operational, simply turned them off to further reduce costs.”

In fact, according to the U.S. Public Health Service/Centers for Disease Control publication, Occupational Diseases: A Guide to their Recognition, 1977, pgs. 319-321, and Fundamentals of Industrial Hygiene and Toxicology, National Safety Council, 1988, Occidental ignored the most fundamental recommendations for worker safety with regards to exposure to toxic chemicals and especially fluorine exposure. “Attention should be given promptly to any burns from fluorine compounds due to absorption of the fluorine at the burn site and the possibility of absorption from burn sites. Gary and his coworkers were never given any medical attention much less provided with adequate protective clothing and equipment.

Of the eight original plaintiffs who were directly exposed to the chemicals, only six remain, but others are coming forward. Two have died: One plaintiff, a non smoker, died of lung and liver cancer, and the other from bone cancer. Gary said the wife and daughter of one man suffering with similar health problems and the neurotoxic damage has developed similar symptoms. He went on to say that many people have died of what he now believes was exposure to toxic chemicals at the Occidental phosphoric acid and fertilizer plants.

“I read in the paper that studies were done in Hamilton County, and they showed that Hamilton County has the highest cancer rate in Florida. Columbia and Suwannee Counties also have very high cancer rates compared to other counties in Florida. Those counties are right next to Hamilton. For me, the article rang a bell because I wondered, why here? Hamilton County is basically a rural, farming county. You would think the air is less contaminated. The overall environment is cleaner. You would think the people would be healthier than in the big cities. The only thing here that is not in some of the other counties is Occidental Chemical Company.

“I wonder whether the water we are drinking is contaminated with chemicals from the leaking gypsum stacks. I worry about the air quality because it’s a fact these chemicals travel great distances and other times, under different weather conditions, they settle over the community. All these things concern me. Now that I know how dangerous some of those chemicals are, I’m concerned for the whole county and the general public. I feel like more studies need to be done by scientists who are not paid by the phosphate fertilizer industry or those government agencies who have done little or nothing over the years.”

After working almost twenty-one years in the phosphate fertilizer industry, Gary Pittman states: “If the facts were brought out in this case, the cat would be out of the bag. They (Occidental) know that I know where all the skeletons are buried. If we can get this information to the public, we could get some things done about the pollution, not only for us, but for the general public. These phosphate fertilizer companies would have to clean up their act. I know the general public is at risk due to sulfur dioxide, radionuclides, fluorosilicates and other harmful fumes being emitted from the plants, holding ponds and gypsum stacks. People are being made sick from that pollution.

” All these things concern and worry me. I thought about reporting the illegal emissions to Florida Department of Environmental Protection, OSHA and the EPA. But I wonder, because you don’t want to report things to the people who already know what is going on. They know people are sick and dying because of Occidental. If they were really concerned and cared about the public, they would have done something about Occidental a long time ago.”

Gary Owen Pittman is also concerned about the lawsuit because he knows that he is going up against a mammoth organization with much to lose. The parent company of Occidental Chemical Corporation, Hooker Chemical Corporation, is no stranger to litigation. Hooker Chemical was responsible for Love Canal (both companies are owned by Occidental Petroleum Corp.). Not only is he going up against Occidental, Pittman and the surviving plaintiffs in the lawsuit are taking on the entire phosphate fertilizer industry.

“It’s hard for us to trust anyone after what we’ve been through. I know Occidental has the power to buy and intimidate people. They could even cause my lawyers problems. They give money to political candidates, and I imagine they help the judges, who think their way, to get elected. All of us know that we’re alone and can’t depend on anyone, except one another.”

ACID MISTS AND CHEMICAL POISONING

Gary Pittman

I started work at the Occidental Chemical Corporation on January 24, 1972 in the Analytical Laboratory at the Suwannee River Complex. I was eighteen-years old and in excellent health.

My first position was that of a Junior Technician, also referred to as a sample preparation technician. I would drive to the mines, wastewater canals or wherever samples need to be taken and prepared for chemical analysis.

The preparation of samples required many different steps. Wet samples of phosphate rock, feed, phosphoric acid and tailings were mixed by hand. Wet samples of rock from the floatation plant contained reagents, fatty acids, amines and ammonia, used to float the phosphate from the sand. We placed them in pans where the samples were baked dry in a conventional drying oven. We never used gloves, and the oven was vented inside the room.

Once the wet samples were dry, we would take them into a grinding room that was very small and unventilated. The grinders were electric and pulverized the rock into a fine powder. We were never provided dust masks or respirators. By the time we finished, we would be covered in dust and had to blow it off with compressed air.

We also secured samples of sulfuric acid, phosphoric acid, Polyphos (an animal feed supplement) and gypsum cake slurry. Entering the sulfuric acid plants, we were exposed to sulfur dioxide. In the phosphoric acid plants we were primarily exposed to silica tetra fluoride gas and toxic vapors from production.

Because I was in an entry level position, I was also the cook when we had to work overtime. Generally, I would cook TV dinners in the microwave oven for the overtime personnel. However, if there were too many people working overtime, I would cook the dinners in the large, conventional drying oven along with the rock samples.

I was promoted to a laboratory technician and analyzed the samples. During that period, I did analyses for fluorine in animal feed supplement and wastewater, analyzed phosphoric acid for metal content using an Atomic Absorption Unit, and general product analyses.

We would start with a sample and add nitric acid or hydrofluoric acid to digest the product. We then placed the sampled on a hot plate under a ventilation hood and boiled them. We poured samples down an open drain in the floor. The reactions would often cause fuming, the release of chemical gases. Chemical fumes in that area were terrible because the exhaust system was not designed to handle the volume of work we did in the laboratory. The fans were belt driven, so when it rained, the belts slipped, and the exhaust fans didn’t work. Sometimes, the fumes were so thick, they took my breath away. The air-conditioning system was a recirculation type and recirculated the fumes.

Occidental provided no safety education or equipment, at that time. The only safety requirement was safety glasses. Respirators, dust masks or gloves were not required or readily provided.

We used to trap fish in the spillway to the retention ponds, clean cook and eat them for lunch or dinner at work. We promptly stopped that practice after seeing a large fish kill from a sulfuric acid spill.

In late 1974, I transferred to the phosphoric acid plants. At that time, I felt as if I was in good health. However, I did have problems with dizziness, difficulty with breathing, some diarrhea, frequent headaches, and chronic colds with congestion.

My first job was as to control the levels in the raw feed tanks transferring phosphate rock from the draglines to the plants. I also pumped the raw matrix into floatation tanks where chemicals were added to separate the silica from the phosphate. The phosphate rock would then be pumped into storage bins to be ground for onsite phosphoric acid production or sold to other manufacturers. The sand (general trailings) was pumped onto a waste stack: these general trailings are radioactive.

In that area, we were exposed to amines, ammonia and phosphate rock dust containing fluorides, silica, heavy metals including uranium and its decay rate products on a daily basis. We were constantly working with the phosphate rock, raw and floated. We breathed the dust, fumes and mists from sprays while taking samples and turning valves. Everyone seemed to be sick with colds, head aches and breathing problems.

Late 1974, I transferred to stores. There, I was an issue clerk at the storeroom. I had to issue tools, parts and general products needed to run and maintain the operation. The stores department was located next to the ball mill where the phosphate rock was ground to a fine powder for the Dorr-Oliver feed supplement plant. Dust from the ball mill was very bad. Walking to and from the parking lot was a source of exposure to hydrogen fluoride, silica tetra fluoride, nitric oxide, sulfur dioxide and general pollution from the plant. At that time, I had frequent cold, congestion and headaches.

I transferred from stores to the Dorr-Oliver phosphoric acid complex as an Evaporator Operator. My job was to bring the phosphoric to 28%, 40% and 50% concentrations. The Dorr-Oliver Complex was the first plant Occidental built at White Springs, Florida in the later 1960′s. I was required to help with other plant duties such as cleaning reactors, holding tanks, gypsum hoppers, the rock room, pipes, fume ducts, and pollution scrubbers. I also had to watch the reaction side of the complex while the operator was busy with other duties. There I set up the pumps, lines, valves and caught samples.

The work environment was very bad at the Dorr-Oliver complex. OSHA had not been formed when the facility was built. We worked in thick acidic fumes and vapors: Silica tetra fluoride, hydrogen fluoride, sulfur dioxide, fumes from defoamers, and gypsum and phosphate rock dusts on a daily bases. Occidental’s safety program was basically nonexistent at that time. Wearing of safety glasses was not enforced, respirators were available on a limited basis and self contained breathing apparatus was not available. I would frequently cough up blood when the fumed were bad. I began to miss work frequently because of terrible chest colds. Some of the old-timers said I had “chemical pneumonia.” Radionuclides were also present as Uranium-328, radium-226, Radon-222, Polonium-210, etc.

In making phosphoric acid, phosphate rock is dumped into a 93% solution of sulfuric acid. The reaction produces silica tetra fluoride gas. When the gas comes in contact with water, it creates fluorosilicic acid. If you breath the silica tetra fluoride gas, when it comes in contact with the moisture in your lungs, hydrofluoric acid is formed leaving a crystalline silica particle. Hydrofluoric acid is the most corrosive acid known. Other fluorine fumes we breathed were uranium hexafluoride, radon hexafluoride and many other types of fluoride fumes created during the acid reaction process. We were also exposed to the gases, vapors and fumes while cleaning tanks, pipes, etc. Solid fluorosilicates and fluoride gases saturated the work areas.

We also had a small laboratory in the control room for analyses. We tested the sulfated for reactor control. The ventilation was very poor. We had to keep barium chloride heated to 198 degrees for hourly testing. The air-conditioning unit was self contained, so it recirculated the stagnant, fume filled air. The heating system was the same, recirculating the air in the room. We had no lunch room, so we sat around and ate lunch while the chemicals were cooking on the hotplate.

At that point in my career, I was unaware that most of these chemicals would cause harm to myself and my coworkers. We were exposed not only to the fumes and vapors from the acid reaction, but also defoamers. The defoamers were used because the sulfuric acid would boil when the phosphate rock was introduced. This would cause the mixture to violently foam and overflow from the reaction chamber. I remember one defoaming agent in particular, AZ-23, an oil-based product. If you happened to get some on your clothes or skin, it wouldn’t come off.

On repair days, we had to clean tanks, reactors, fume ducts and the pollution scrubber, etc. This was nasty work that required entering confined spaces for long periods of time to clean out solidified fluorosilicates and gypsum scale. We had to use air chisels to chip out way into the vessels while tossing chunks out by hand. The sludges had to be shoveled out by hand. All of these toxic materials were dumped into the evaporation ponds atop the gypsum stacks.

Clean up was a dirty, nasty job. There was no ventilation and no tests were done to see if the oxygen content would support life. When my wife washed my clothes after clean up days, they would fall apart because of the fluorosilicate dust I picked up.

The Dorr-Oliver complex was shut down due to a sagging sales, and I was laid off for six weeks. My health was about the same: Chronic colds, congestion and headaches with some dizziness and trouble breathing.

I went back to work as a solvent extraction operator in 1977. As noted, I had already held many positions at Occidental and proved to be a competent worker. Occidental was expanding the product line and building new complexes to accommodate production of the products. We were experimenting with new processes, facilities and ideas.

The Solvent Extraction was an experimental facility built to extract iron, aluminum magnesium and mainly aluminum out of phosphoric acid. Occidental planned to produce superphosphoric acid and ship it around the world. There was only one major problem. The metals cause the superphosphoric acid to crystallize. The Solvent Extraction (called SX) plant was designed to remove most of the metal contaminants.

I was the “A” operator in this experimental SX facility. We mixed several chemical reagents with the phosphoric acid which were supposed to extract the metals. I was exposed to these chemicals daily. A supervisor told me that mixtures of these chemicals with phosphoric acid were hazardous, but I was never issued any personal protection equipment. I later discovered that the chemicals were flammable as well as toxic.

The chemical was Di-Nonyl-Naphalene-sulfonic acid. It was mixed with kerosene and then added to the phosphoric acid. Sulfuric acid was added in the process. The solvent had a muddy color and a peculiar smell.

The process worked, but Occidental was having difficulty in disposing of the toxic wastes and abandoned the project. Later, the same result was achieved using a drum-filter process. At that time I began suffering with severe dizzy spells with frequent colds, breathing problems and headaches.

I was transferred to the Prayon complex built at White Springs, Florida as an evaporation operator. There, I operated five low pressure evaporators that would bring the acid to various concentrations. I was required to help change filter cloths and cleaned filtrate tank lines, fume ducts and pollution scrubbers. I also took and analyzed samples for superphosphoric acidic concentration, sulfate levels and other contaminants.

The Prayon complex was much larger then the Dorr-Oliver plant. In spite of the fact that it was a new facility, the working conditions were about the same. We were exposed to the same toxic chemicals possible at a greater concentration because the plant was larger.

Occidental’s safety program was still very poor, but OSHA was beginning to make visits and inspections. Respirators were available on a limited basis, but we had no self contained breathing apparatus. The only required protection gear at that time was a hard hat and safety glasses.

Repair days brought exposure from breathing and contact with the acids and chemicals. No tests were done for oxygen levels. The vessels were normally hot, there was no ventilation and workers would often pass out due to the heat and fumes. I have seen this happen, many times. I would often cough up blood after cleaning days.

Next, I went to the Hemihydrate phosphoric acid plant as an “A” operator for a new process. My job was to control the reaction and filtration processes. The process was complex and consisted of a rock slurry tank, dissolver reactor, crystallizer reactor and filter feed.

Phosphate rock, water and sulfuric acid were mixed together to form phosphoric acid slurry. This concoction was pumped to a tank where the gypsum solids were filtered out. The fumes were the worst I had ever experienced at Occidental. They were so thick, and acidic, my skin would start burning.

The excessive fuming was due to the nature of the Hemihydrate process. With the other processes, the phosphoric acid is about a 28% concentration at 165-180 degrees Fahrenheit. With the Hemihydrate process produces a 40% concentration at about 205 degrees. The process generated excessive fuming and release of silica-tetra fluoride and hydrogen fluoride gases.

Since the Hemihydrate process was new, we were basically flying by the seat of our pants and learning something new every day. At first, we had bad foaming problems in the dissolver reactor. We had to use very large amounts of defoamers to keep foaming over at a minimum, but it was still a problem in the early days of operation. We were always sloshing around in acid. I was buying a new pair of shoes every two months. The acid would literally eat the shoes off our feet.

We would develop acid sores and rashes on our arms, hands and feet. I remember one day when I was assigned the task of cleaning a filter hood along with another employee. White, powdery fluorosilicate dust was everywhere. As we were cleaning, the powdery dust would fill the air and cover us. The weather was hot, we pulled a six-hour stint and we were sweating profusely. When the fluorosilicates hit the sweat on our bodies, they formed fluorosilicic acid. If we didn’t wash it off in time, blisters would form.

Going home that evening, my clothes began to fume so bad I couldn’t see. My eyes were also burning. I had to roll the window down in order to see the road.

Later, I was promoted to supervisor of shift workers at the Prayon and Hemihydrate plants. At times, the position was worse than being a shift worker. Aside from all the clerical and supervisory duties, I found myself in the middle of spills, and foamings or helping patch leaking pipes or pumps.

In 1978, I returned to the Dorr-Oliver complex as a supervisor for a restart with a new computerized control room. OSHA was citing Occidental on a regular basis for safety violations. Occidental was attempting to improve the company safety program. The Florida Department of Environmental Regulation was also investigating Occidental for emission violations. They were emitting fluorides at almost ten times the level allowed by law. The hydrogen fluoride emissions were eating the paint off cars and etching the glass on our vehicles in the parking lots. The Dorr-Oliver sulfuric acid plants were also emitting large quantities of sulfur dioxide. At that time the only safety gear required was a hard hat and safety glasses.

Occidental was building a new chemical complex at what is now called Swift Creek. In late 1979, I was transferred to the Swift Creek complex to help with the start up. I left Occidental in 1980 to manage our small, family farm until small profit margins drove us out of business in 1985. I returned to Occidental in 1985 as a shipping supervisor. I was responsible for unloading raw materials and loading sulfuric acid, phosphoric acid and super phosphoric acid into railroad cars.

The worst chemical exposures in this area were to sulfur dioxide and sulfur trioxide from burning sulfur. We melted the solid sulfur in railroad cars by attaching steam lines to coils inside the cars. The super heated steam melted the sulfur to a red hot, molten state. At that point we could unload the cars into launders below the cars. The sulfur is used to make sulfuric acid.

Sometimes the railroad cars would catch on fire and the only way to extinguish it was to climb atop the car and shut the dome lid. This would cut off the oxygen.

When popping the dome lids, we would always get a whiff of hydrogen sulfide, a deadly gas.

In 1985, I found myself back as a supervisor at evaporation purification. There, I oversaw the last purification steps of superphosphoric acid before it went to the customer. The acid was concentrated to a 70% solution.

We received our low grade phosphoric acid from the Hemihydrate plant where it goes through several processes. We treated the acid with Synspar (synthetic fluorspar) to remove iron, aluminum and magnesium among other steps in the evaporation and purification process.

We made the Synspar by adding lime dust to evaporation pond water containing about 15,000 parts per million of fluorine (hydrofluoric and fluorosilicic acid) in a reaction vessel. The reaction drives of carbon dioxide leaving calcium fluoride and sodium silicofluoride. Calcium fluoride is the Synspar which is separated and dewatered in a centrifuge. We were exposed to fluorides, defoamers, and acid fumes and vapors for 8-12 hours a day.

September of 1986, a rash began to cover my arms, hands and back. It was a round circular rash that would start out small and grow leaving my skin white and scaly. The rash was eating me alive. My neighbor was a doctor and I asked him about it. He said that he had never seen anything like it before, but it might have been caused by a reaction or be mycotic. He prescribed some medicine and the rash went away. I missed work several days on that occasion.

Several years later, my right hand became swollen. I went to the doctor, and he said that I had a hairline fracture above the pinky finger. I had not hurt myself. It healed in several weeks.

As I continued to work in evaporation and purification, I experienced frequent colds, neck pain, dizziness, chronic fatigue and breathing problems.

About that time Occidental shut down “A” pollution scrubber. We had two pollution scrubbers, “A” and “B.” The explanation from management as to why the scrubber was shut down was, “they are not needed.” That surprised me because I knew the permits from the state required that both scrubbers be in well maintained and tested by the state inspectors on a yearly basis.

“A” scrubber removed some of the more toxic fumes and it was evident when it was not running. I was afraid to report what Occidental had done because I would have lost my job. The “A” scrubber was down for three years until the manager retired and a new person came. When our new boss took over, the scrubber was put back on line.

Even the cooling stack tests for fluorine emissions done by the Florida DEP and OSHA were “fixed”, for the most part. The DEP and OSHA had to notify Occidental before inspecting the complexes. All the pollution scrubbers were cleaned, and we used fresh water instead of evaporation pond water. The next step was to have defluorinated animal feed supplement dumped into the reaction vessels and raw phosphate slurry following that so if the inspectors took a sample the fluorine content would be right. The cooling stack tests would be complete with a clean bill of health before the raw slurry was dumped into the reactors. This was standard operating procedure when Occidental was to undergo emissions testing.

In 1991, I woke up feeling dizzy and nearly passed out. I felt as if my heart was skipping beats. Frightened, I went to the emergency room at Lakeshore Hospital in Lake City, Florida. They checked me out, did an EKG and drew some blood. The doctor came back and said that he thought I had Lyme’s disease, but the tests came out negative. I was out of work for several weeks and lost twenty pounds.

I was promoted to an assistant superintendent in 1991 and seemed to be doing better health-wise. My new job was very challenging. I made most of the decisions regarding problems around the plant.

With the fall of the Soviet Union we had lost a large contract supplying them with superphosphoric acid. The entire industry was depressed, and we were trying to find new ways to make phosphoric acid at less cost. The company was downsizing and we were doing more work with fewer people.

In late 1992 and early 1993, I began working with different types of scale inhibitors and slurry flocculants. These were known carcinogens. Warnings were on the labels. I don’t remember the names, but I requested material data safety sheets for our files.

In may of 1993, my feet became swollen and I could barely walk. I was also having dizzy spells, suffered with episodes of confusion, dizzy spells, heart palpitation and chest pains. I went to a doctor in Valdosta, Georgia. They drew blood and did an EKG. The doctor said that I had a heart attack, but not recently.

My last working day at Occidental was 21 May 1993. That is when I went on short term disability for two years. I returned to the doctor to learn that I had some type of muscle destructive process happening. My CPK enzyme levels were over 5,000 which is very abnormal. The doctor told me that there was nothing he could do except recommend a specialist.

I went to see the specialist. They did a muscle biopsy, reviewed my blood tests, medical files and said that I had a muscle disease and would never be the same. He called the disease polymyositis and said that I had major muscle damage. The prognosis was if my CPK levels stayed down, I would regain some strength. After being out of work for six months, I had to go on long-term disability.

After about one year, my condition improved some, but not to the degree the doctor thought. I saw another specialist in Tifton, Georgia. After reviewing my medical records and running tests, he said that I had some form of myopathy, but could not label the type. Later I went to the Environmental Health Center in Dallas Texas and was diagnosed with toxic brain syndrome (toxic myopathy).

Today, I suffer with many disorders including obstructive pulmonary disease with emphysema, toxic brain syndrome, irregular heart beats, arthragias, hypertension, loss of memory, loss of balance, abnormal liver and sores on my hands, legs and behind my ears.

Like so many people, I was naive and always thought that Occidental had my best interest at heart. However, in view of my experiences during the twenty years I worked for Occidental Chemical Corporation, I learned the hard way: Standard operating procedure for Occidental management was based on falsehoods, deceit and with the attitude that they can do no wrong.

THE CLEAN JOB

Clinton Vann

I started work at the Occidental Chemical Corporation as a Junior Laboratory Technician in 1966 at the Suwannee River Complex. I was 18 years old, earned two dollars an hour and did the usual sample worked described in Gary Pittman’s account.

When I first started at the Suwannee River Complex, the lab wasn’t finished. We had to dry samples on hot plates in the lab with only two windows for ventilation. In 1967, Occidental bought a large drying oven, but the fumes were still vented into the lab where we were doing analyses. The only safety equipment we had back then was [were] safety glasses. Gloves, respirators and dust masks were not supplied to us. We were constantly exposed to reagents used for analyses, vapors from acidic reagents reacting with samples, fumes from boiling reagents and dusts from grinding phosphate samples.

It was sort of ironic that we cooked our meals along with the samples drying in the sample oven. At that time, the practice was out of necessity. We didn’t have a designated eating area, and many times, we had to eat while were doing analyses. It wasn’t unusual to be eating a sandwich and working at the same time. The samples contained ammonia, amines, fatty acids, fuel oil, kerosene, sulfuric acid, fluorine gases, etc. Vapors and gases from these chemicals were given off during testing procedures.

In the early years, we used glass jugs to store bulk reagents. I remember one time, a five-gallon, glass container of a nitric/hydrochloric acid mixture broke. The contents spilled over a lab-tech’s legs and feet. It immediately dissolved his socks and shoes. The fellow almost passed from the acid fumes. Another time a glass container of ammonium hydroxide hit the floor and busted. We had to evacuate the whole lab.

I worked as a sample tech for about three years before I was promoted to a lab technician and began doing wet analyses. We used nitric acid, hydrochloric acid, ammonium hydroxide, acetone, xylene, triethanolamine, potassium cyanide, sodium fluoride, trichlorethylene, etc. We used the cyanide in a manner which I now know was very dangerous. We added acid to a cyanide solution that fumed cyanide gas. There was no adequate ventilation so we would turn our nose away because the fumes were so strong. We were making the same cyanide gas used to execute prisoners.

The ventilation in the lab was very poor, even under the fume hood. We also did many analyses not using the fume hood. One such test was the distillation method for determining fluorine levels in the phosphate rock. If the conditions were not right, fluorine gases would be created. We also used hydrofluoric acid in this procedure.

Located outside the fume hood, we had a high temperature oven we called a “mini pilot plant.” We used this device to simulate the Polyphos (animal feed supplement) process where fluorine is driven off the phosphate rock by heating it to a molten state. The Polyphos complex could not run unless we did these test first to determine how long the rock had to be cooked to bring the fluorine levels down to where they were acceptable by the U.S. Department of Agriculture.

Most analyses were done by dissolving samples in nitric, hydrochloric or perchloric acid on hot plates under fume hoods. The exhaust systems did not perform properly. Cooking samples in perchloric acid under the same fume hood was dangerous. Perchloric acid fumes form an explosive compound on the inside of the fume hood. Fortunately, we never had an explosion, but I knew someone who did experience an explosion. His name was Charles Thornton. He owned Thornton Labs in Lakeland, Florida; he was severely burned when the hood in his lab exploded.

The air-conditioning in the lab was a closed loop system. All it did was recirculate contaminated air. We were sure of this because we would clean the glass on interior doors at night before we left. Come morning, the glass would be coated with sticky dust again. We used to comment about the lab conditions saying we had a good clean job in the laboratory. Little did we know that we were exposed to dangerous chemicals and the consequences of that exposure. As far as I know, they are still using the air-conditioning system.

We were exposed to chemicals both inside and outside the lab. Like most everyone else who worked at the complex, I have had my car painted twice because acid fumes etched the paint on my car. Occidental still says that the pollution will not hurt you.

1973, I was promoted to Shift Supervisor at the Suwanee River Complex Analytical Laboratory. Most of my time was spent in the lab area troubleshooting problems and training seven lab assistants in new procedures. I was also responsible for performing maintenance and calibrating lab instruments.

By 1979, I was promoted to Lead Analyst of a Special Services Group and transferred to the Jacksonville, Florida port terminal. There, I did analyses on bulk shipments of phosphoric and superphosphoric acid. I was first trained in the use of respirators at that time.

In 1982, the Special Services Group was eliminated because of downsizing, and I went back to the position of a shift analyst at the Swift Creek complex.

In June 1983, I went for a routine physical at the Riverside Clinic in Jacksonville, Florida. Test results showed that I had liver abnormalities. They continued testing me through 1985, and the liver function abnormalities persisted. Dr. Weitzner and Dr. Merrel of the Riverside staff recommended that I no longer work in areas where I would be exposed to hepatotoxins. On June 26, 1986, I was assigned to work outside the lab after my superintendent and Safety Superintendent discussed my situation. This was done during the time interval required for the company doctor to review my records.

On July 15, 1985, Dr. Zavon, Occidental’s corporate medical consultant, sent the slides from my liver biopsy to a Dr. Cushner at Stoney Brook University in Long Island to review. Dr. Cushner was the dean of the college and a medical pathologist. Dr. Cushner said that he didn’t see much in the slides. The doctors in Jacksonville, had already noted that I had changes in my muscle enzymes levels. Consequently, on September, 10, 1985, Dr. Zavon telephoned the doctors in Jacksonville and persuaded them to “ease off” what he considered an “over diagnosis.” I was back in the laboratory in November, 22, 1989 doing routine work. However, there was one limitation, I was not to perform analyses using organic solvents like methanol, ethanol, acetone, etc.

In 1990, my health problems began to worsen, and I was diagnosed with muscular dystrophy. This diagnosis was basically confirmed by three doctors in spite of previous medical records stating that I had suffered with idiosyncratic chemical hepatitis. My condition continued to deteriorate until I was totally disabled in 1993.

In 1991, when I was diagnosed with a degenerative muscle disease, I asked my superintendent about the possibility of being transferred to a less stressful and demanding position. He spoke with the Technical Services Manager. Both my superintendent and the Technical Services manager said there were no positions available. Several years later I discovered that the Technical Services Manager filed a suit with the EEOC because he did not get a job he wanted. Occidental wound up placing him in the position he requested.

My last day working for Occidental was February 28, 1993. I was never offered another position at Occidental in spite of my twenty-seven years there.

In a report, Dr. Weitzner (Riverside Clinic, Jacksonville, Florida) said that the test data was consistent with the toxic effects of drug use. But I had never used drugs. I told him it had to have been the chemicals. I then asked him if he would relate the solvents to my liver damage. Dr. Weitzner said that he would not say that my liver damage was caused by chemical exposure in the workplace.

The only reason I could determine for Dr. Weitzner’s reluctance to state that chemical exposure could have caused my liver problems was that Riverside was contracted by Occidental to supply medical services to company personnel. The lawyer representing my workman’s compensation case had to force Riverside Clinic to release my medical records with a court order.

In 1994, doctors at the Mayo Clinic in Jacksonville said that I might have passed “something” on to my daughter and son. They said that my family history suggested that, but they were unsure. During my infancy I had a mild case of polio, but that disease is not hereditary. Tests proved that my family (granddaughter) has no hereditary health problems. I did a family tree going back over one-hundred years including more than one-hundred people, and there were no health problems resembling mine. The doctors said that I had also these problems since I was in high school, but how could I have worked for twenty-seven years on the verge of total disability?

In 1997, I went to the Dallas Environmental Health Center for toxicological testing and a spectrographic brain scan. The results showed neurotoxic damage. Occidental sent the findings to a Dr. William George of Tulane University in Louisiana and Dr. Ronald Gots, Bethesda Maryland. They concluded that none of the chemicals I worked with could cause muscular dystrophy or the health problems that many people who worked for Occidental now suffer with. However, there are other people who worked for Occidental who have the same symptoms. I, Jesse Nash and Gary Pittman have all been diagnosed with toxic brain syndrome at the Dallas Environmental Health Center.

Gary Pittman was first diagnosed as having Lyme’s disease, then non specific muscular disease and finally with toxic brain syndrome. They said that Jesse Nash had Lupus and then palindrome arthritis. Many others who worked for Occidental are similarly ill, and I wonder how many of them have been misdiagnosed by doctors working for clinics contracted by Occidental.

In 1998, I retained a Miami-Ocala, Florida-based lawyer, Henry Ferro. One day before he believed the statute of limitations ran out, Ferro filed a toxic tort lawsuit on my behalf. The lawsuit was sent to Federal court. I believe that Ferro was threatened by Occidental, because without my consent, he filed a motion to dismiss himself as my attorney. I had to petition the judge to dismiss my case without aid from an attorney.

Along with Gary Pittman, I have done extensive research into the long-term toxic effects of the chemicals and substances that were prevalent at the Occidental chemical complexes. Many of the toxic effects of those chemicals have been known for some time. Occidental management had to have known that they were systematically poisoning workers by not providing proper safety equipment and education regarding the handling of those chemicals and substances. However, Occidental has the money and where-with-all to hire attorneys, experts and doctors who will say that breathing cyanide gas will not hurt anyone except murderers in a gas chamber.

FUMES AND TOXIC SLIMES

(Billy Baldwin’s Story)

George Glasser

“Billy is the type of person who gets up early in the morning and goes to bed about 11:00 p.m., but in September 1993 he would come home from work and go to bed. Living with Billy for more than thirty years, I knew something was wrong. Billy was tired all the time. He had headaches, nausea and looked like a ghost.

“Finally, I asked him to go to the doctor, but Billy said he would lose his job if he took off from work.”

Billy Baldwin came home from work on the afternoon of November 13, 1993 and said he couldn’t take it any more. Charlotte took Billy to the emergency room al Lake Shore Hospital in Lake City Florida. He was admitted for severe anemia and remained hospitalized for three days. A blood test and bone biopsy were performed, but the hospital doctors said they could find nothing unusual.

Billy was given a prescription for very large daily doses of vitamin B12 with frolic acid tablets for one year. When Charlotte went to the druggist, he asked who had written the prescription. “I asked what was wrong, and the druggist said that athletes didn’t take that much B12. He then said that he would have to verify the prescription with the doctor.”

After two weeks, Billy’s condition didn’t improve, and he still was very anemic. He was then referred to Dr. Vernon Montoya in Gainesville where again they drew blood and took a bone biopsy. When the results came back, the doctor asked Billy how he managed to walk into the office.

A few days later, when the results from the bone marrow tests came back from the laboratory, Dr. Montoya called Charlotte. “I took the phone and asked what was wrong. Dr. Montoya said that we would discuss it in the morning, and I questioned him further. Finally, he gave in and told me that Billy had leukemia, the worst type. It broke my heart.”

Charlotte Baldwin’s account is only one of many from the wives of men who have worked at the Occidental Chemical Complexes in Hamilton County, Florida. Billy is a stable person, the father of two daughters, and he has only had two jobs during his adult life with time out to go to Vietnam in 1968. He started with Occidental in 1979 as a laborer on the float crew at the mines. Later, became a “whencher” who lays and repairs pipes that transport the phosphate slurry to the phosphoric plants and tailings to the phosphogypsum stacks.

It was usual for Billy to wade waste deep in radioactive sludges and toxic slime from the production and mining wastes. “When they mine the phosphate rock, it is dumped into a well pit and broke up with high pressure hoses. From there the slurry was transported through pipes to a washer where the phosphate was separated from the sand and clay. Sometimes the pipes ran three or four miles to the washer. Many times, We had to lay those pipe lines across toxic slime ditches. The pressure from the pumps was so great that it wasn’t unusual for the 18 inch steel pipes to blow out. We had to work waste-deep in the mud and slime.”

If the washer was nearby a phosphoric acid plant, the toxic, radioactive waste water was used. In the pipes, there are flow meters that adjust the flow rate of waste water being delivered to the pond and detect levels of radioactivity. When the men were working on the lines, the flowmeters were supposed to be shut down, but many times they were not. Not only was there slime containing uranium and its decay rate products, but there were all the solvents, fluorides, flocculants and acids associated with the production of phosphoric and sulfuric acid.

Occidental float crews were given no special protective gear, clothes, dust masks or respirators. “Close to the chemical plant or washer, the plant water would be mixed in with all the phosphate, mud and water we were working in. Sometimes, we would be up to our waists in the slime and mud for the whole shift. It smelled of chemicals and stagnant water, a stinking blue-grey slime with an oily slick floating on top of it.”

As the phosphate rock is broken down with water and floated, slimy clay sediment remains, referred to as a mud ball. This is sucked up through a 24-inch steel pipe and shot into a settling pond. The mud ball sits there for a few days until it becomes firm enough to extend more pipe across. Often equipment used would become mired down and float crews were required to wade out in the radioactive sludge and free the equipment. This task was completed by the crew no matter if it took one-hour or twenty-four hours of being waist deep in the sludge.

Evaporation from the contaminated slimes, water and mud carry with them the toxic substances contained in the waste. Radon, a gas and decay rate products of uranium, also drifts off in the evaporation process. Alpha emitting radionuclides do not pose a significant threat outside the body. But when ingested or inhaled and metabolized, they pose a significant threat. Radon is only one of many decay rate sequences of uranium-238. In 2.86 days it decays to lead-210 which acts like calcium in the body and is a bone seeker. Lead has a half-life of twenty years before it decays to polonium-210. Polonium-210 emits five-thousand times the alpha radiation as the same amount of radium. The half-life of polonium-210 is 138 days. Beta radiation emitting radionuclides like lead-210 which has a half life of twenty years (accumulates in the bone) are also dangerous when ingested and metabolized in the body.

Also, it is likely that radium and uranium, alpha emitters, were converted to gaseous fluorides as the hydrogen fluoride was evaporated from the pond water. Breathing the radioactive, gaseous fluorides would possibly act to potentiate the effects of the radionuclides. As with fluorosilicates, a reaction would occur when the fluorides came in contact with moist bronchial or lung tissues. Separation would occur forming hydrofluoric acid and the radionuclide. The hydrofluoric acid would dissolve the lung tissue leaving the radionuclide to be carried into the blood stream and delivered to target organs.

Leukemia is associated with exposure to radiation. Leukemia is also a disease that is associated with young people. Billy was in his late forties. Interestingly, people living near phosphate mining operations and processing are twice as likely to develop leukemia and lung cancer.

Billy also spent time at the Suwannee River Phosphoric Acid Complex and related: “They had a reduction in the work force. Instead of laying me off, they sent me to work in phosphoric acid production. At that time, they had shut down the reactor, and we had to clean it out with chipping hammers the scale was so hard. It was so hot and the fumes were so thick in the reactors that we could only work in thirty minute intervals. We were never provided with respirators. We couldn’t wear the rain suits provided to us because it was so hot. We would have passed out from heat exhaustion; we were working Twelve-hour shifts.

“We also had to clean the pollution scrubbers. There was white, powdery fluorosilicate and phosphate dust all over. We sprayed the walls with a high pressure hose. We had to use the acid resistant rain gear in there, but we had no respirators. The acid water would splash all over us and get inside the suit, We had to take showers all the time. And the fumes were very bad.”

Fluorosilicate and phosphate dust were so thick in the production areas, the men would have to sweep the toxic dust into wheel barrels which were dumped onto a conveyer belt. The dust was so thick in the air, the men would “spit and cough it up.” Billy stated that his skin turned ashen during his assignment at the phosphoric acid complex.

For a time, I worked at the ball mill where they grind phosphate pebble to be processed among other jobs. On the survey crew, we mostly surveyed raw phosphate fertilizer at the Suwannee River granulation complex. They were all dirty and dusty jobs.

The environment was even less important than the employees to Occidental management as documented by Billy Baldwin: “I worked on a survey crew twice at Occidental. We cut a line through the woods around washers at the Swift Creek and Suwannee Complexes. The washer pits were filled with steel drums, paint cans, break fluid, spray cans and chemical soaked wood from the acid complexes.

They covered the pits with a certain amount of tailings sand, then they would dump a measured amount of mud ball waste. This stuff was contaminated with everything used at the complexes. We would have to survey to make sure each level of sand and mud was about two feet thick. After we were finished, they planted pine trees over both dump sites. There were a lot of different chemicals covered up at both dump sites. We worked on those dump sites for a long time.”

Billy also states that it was common to see dead fish and birds around the incoming pumps at the washing pits. “Going into the Swift Creek complex, I used to see catfish with blisters on their backs and back. We hardly ever saw any birds around the ponds, but if one would land and take a drink, they would start flopping around and die. Nothing much lived around those ponds. The trees and plants were all burnt and dead from the acid fumes.”

The contaminated mud and sand tailings were also used to reclaim the strip-mined land. “After the operation was finished, pine trees were planted over the reclaimed land,” said Billy. “The tailings and meat ball they used to reclaim the pits had a little bit of everything in them.”

Accounts from other Occidental employees cite birds falling out of the air when passing over the complexes because of sulfur dioxide emissions. “Birds would fly into the reddish haze from the sulfuric acid complex and just drop out of the sky like rocks.”

In poor, rural counties, employees were a renewable resource. In spite of the ultimate price, most people are grateful to have good paying jobs and say nothing about the working conditions. At the Occidental Chemical Complexes in Hamilton County, Florida, exposure to chemicals, radionuclides and acids were all part of the job description for their workers. The resulting adverse health effects could be debated with Florida Judges, Department of Environmental Protection and Department of Health who are all sympathetic to the positions and well being of the phosphate fertilizer industry in Florida.

In essence, if workers wanted to keep their jobs, they do what they were told and don’t make waves. The employee’s safety and health were not even a minor consideration when it came to profitability by Occidental Chemical Corporation bean counters.

In Florida almost everyone cooperates with phosphate fertilizer manufactures. The blood sample and bone marrow biopsy was taken from Billy Baldwin at the Lake City hospital: Charlotte Baldwin said when she requested the results, the staff said they had lost them. The extremely low white blood cell level would indicate to any competent doctor that Billy had a serious problem and further tests should have been done. The physician prescribed massive doses of vitamin B12 for a period of a year.

No tests were done for toxic substances in the bone marrow or blood when everyone knew that Billy worked at the Occidental chemical complexes and was exposed to toxic substances. Thus far, all the workers interviewed have stated that when they went to local hospitals for emergency treatments or to doctors, no one ever did any testing for toxic substances in their blood, hair or urine. It was common knowledge that they worked for Occidental and were exposed to toxicants on a daily basis. No questions were ever asked.

When Billy Baldwin visited Dr. Montoya in Gainesville, he was on the verge of death from leukemia. The physician at the Lakeshore Hospital in Lake City had prescribed vitamin B12 and folic acid which was correct for a normal case of anemia, but Billy had leukemia and death was knocking at the door.

In reading the accounts and speaking with other employees, one comes to realize that misdiagnosis was the norm. Jesse Nash was diagnosed with Lupus, and Gary Pittman with nonspecific myopathy when both were suffering with toxic brain syndrome. This leaves one wondering how many other workers were misdiagnosed, prescribed painkillers or vitamins and died. How many death certificates suggest some generic cause of death such as heart failure or stroke?

BRIMSTONE AND HEAVING EARTH

Jesse Nash

Jesse Nash’s account touched me because we had much in common. Jesse, is one of those guys who has been around. He went over to Tel Aviv, Israel and volunteered as a fire fighter/emergency medical technician during the Gulf War and received commendations. He is a certified cave diver, open water diver, amateur archeologist and outdoors man. Jesse has done a little of everything including a stint as a Highway Patrolman, but today he cannot mow the lawn on a riding lawnmower without suffering from swollen joints and disabling pain for weeks. Jesse is disabled and suffers with toxic brain syndrome, palindrome arthritis and has high levels of radionuclides in his system.

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My first experience with chemicals and chemical exposure was when I began working for Occidental Chemical Corporation’s Suwannee River Chemical Complex in 1979. Hired as a temporary laborer, I was scheduled to work a minimum of twelve hours a day for twenty-one days during a sulfuric acid turnaround. We replaced or repaired all of the damaged or worn equipment. (A turnaround is a major overhaul of the facility that is done every two years at most sulfuric acid plants)

As temporary laborers, we had to remove spent vanadium pentoxide catalyst (a toxic metal) from the plant converter. A converter is a four-story sealed tank (called masses). Each floor is covered with about two feet of vanadium pentoxide. Extremely hot sulphur dioxide is passed through the beds and is converted to sulphur trioxide that later is made into sulfuric acid.

Back then, the work wasn’t easy. We had to crawl through 24 inch hatches. There was no ventilation, and safety was not a priority at that time. Sweating and breathing fumes, we had to remove the spent catalyst in five gallon buckets, lug them to one of the hatches and dump the buckets into a hopper. All we were issued were hard-hats, safety glasses and dust masks. The masks clogged quickly because of the sweat, moisture in our breath and thick dust present at all times. Sulfuric acid was formed when the sweat came in contact with the dust caked around the edges of my mask and burned my face.

From the third day of turnaround until the converter was refilled with vanadium pentoxide, I stopped by the clinic each morning so the nurse could dress the burns. All I could wear was a hard-hat with a face shield because the bandages were so bulky. Now, I wonder what those dust and fumes were doing to my lungs.

I guess I did all right, because a supervisor, Joe Crosby, called me aside and said that he recommended me for a permanent job. In 1979 he died at about forty-years old, I heard that his lungs were shot. There was another fellow, Buck White, who was hired from the same temporary crew as a weighmaster developed cancer and blew his brains out. Now that I look back, I should have figured out that something was wrong around there, it seemed like people were dying or sick all the time and then there were all the deaths over the years.

One week later, I was hired as a permanent employee at Occidental as a Bulk Handler in the shipping department at the Suwannee River Complex. My first job consisted of loading 93% pure sulfuric acid into rail-cars and trucks and then in the sulphur area. Several months later, I was promoted to supervisor.

Sulphur is shipped to the plant in solid form contained in steam jacketed rail-cars. My job was opening the rail-cars and hooking up the steam pipes to melt the sulphur. Forty-eight hours later, the sulphur was melted, and the molten sulphur was dumped into launders and then pumped into heated storage tanks. I had never heard of hydrogen sulfide and no respirators were ever given to us.

One time, I opened a dome lid and was overcome with the noxious fumes. Afraid that I would pass-out and fall onto the tracks, I laid down, rolled over and clung to the hand holds. When I finally caught my breath, I climbed down off the car. I thought it was a gas leak from one of the four sulfuric acid plants in the area. When I got home, I took off my jacket, and noticed that it was full of tiny holes.

Sulphur fires were as common as the sunrise. They usually start because sulphur fibers hanging on the open dome lids of the rail-cars produce static electricity if a slight breeze is blowing. During unloading operations, sulphur spills onto the ground. The ground around the yard is a dirty yellow. Locomotives pulling rail cars pass and ignite the sulphur on the tracks. People used to drop cigarette butts and that would set off a sulphur fire too.

The worst part about sulphur fires is that you can’t see the flame. The fires are spotted by a plume of bluish smoke, if we saw them. Otherwise, the sudden reaction of coughing, gagging and burning eyes sent everyone running for the water buckets. We didn’t have any running water so we had to grab five gallon buckets and get water from a nearby ditch.

I got tired of the sulphur fires and noxious fumes. I applied for a transfer to work as an oiler at the Swift Creek mine. I got the position on #5 dragline. Draglines are mammoth earth moving machines with forty-five yard buckets that strip-mine phosphate rock. I was happy to get away from the fumes of the sulphur plants and train yards. On dry days, the air was thick with dust at the mines, but I was so happy to be away from the fumes and acid burns, I never thought about there being any health risk at the mines. Later, I read the Material Safety Data Sheet (MSDS) on all the contaminants contained in phosphate rock: cadmium, chromium, lead, uranium, silica, fluorine, mercury, etc. On pages 6 of 8 of the MSDS, I saw where cadmium and chromium cause cancer in the State of California. Guess I’m lucky to be living in Florida! According to the Florida Department of Health, those substances don’t cause cancer in our state. It must be something about the weather.

On August 16, 1979, I was promoted to shift supervisor in the Material Handling Department at the Swift Creek Complex, which was still under construction. The Swift Creek Complex was built specifically for production of phosphoric acid to meet the terms of Armand Hammer’s twenty-year trade agreement with Russia. I spent the rest of my career at the Swift Creek Complex.

To understand the nature of my exposure to toxic substances from phosphoric and sulfuric acid production, you have to appreciate the volumes we produced. Five-thousand tons of 93% pure sulfuric acid was produced each day that was used in the acidulation of phosphate rock.

The sulfuric acid is mixed with ground phosphate rock slurry where a reaction takes place producing toxic fumes, waste gypsum and about 34% phosphoric acid. The SPA (70% phosphoric acid) was so thick, so condensed that it must be kept at over 110 degrees circulate and pump. We produced 1,400 tons of phosphoric acid a day and 7,000 tons of radioactive gypsum waste. There are mountains, gyp stacks, made with the waste gypsum.

The Swift Creek Complex went on line in late 1979, and the start-up was not without problems and chemical exposures. To charge the evaporators that concentrate phosphoric acid, my department was required to unload rail-cars of phosphoric acid into an open rail-car wash sump (an open tank with a steel grate over the top). We then transferred it back to the evaporators. Fumes from the phosphoric acid were overpowering.

I was supervising a crew of day laborers who had never been in a chemical plant. Fibercast lines in overhead bridges would often blowout and spew out thousands of gallons of hot acid splashing onto the ground. Choking on the fumes and with only knee boots for protection, we waded into the hot acid. I remember dumping countless fifty pound bags of lime to neutralize the acid.

The sulfuric acid storage tanks are huge, more than thirty feet high. It is the supervisor’s task to enter the tank first and sample the air for oxygen and explosive gases. We had to enter the tanks numerous times to do spark tests, check the rubber lining and clean sulphate sludge buildups.

Sulfuric acid storage tanks would accumulate about 6 inches of sulphates on the bottoms. Again, we would company laborers to do the cleaning. It was like cleaning up after a muddy flood. We used squeegees, pushing the sludge into five gallon buckets and filled 55 gallon drums. The drums were dumped into the one-hundred acre cooling/evaporation pond.

Cleaning the tanks is a messy job. We sloshed around, ankle deep, in the acidic sulphates filling five gallon buckets. The sludge splashed all over the ground. The stuff will eat the soles off your shoes, so I had the men dump lime on the spill area and place a piece of plywood over the mess. Pretty soon the reaction of the lime with the sulfuric acid sludge started the plywood smoldering. The laborers were hopping around like chickens on a hot plate. The reaction also caused fuming and gave off sulphur dioxide that wasn’t any too pleasant.

In the sulfuric acid storage area, there was a large, brick-lined sump for transferring the acid. So much acid had been spilled in that area over the years that the ground was totally saturated. When the acid would hit the aquifer, a reaction would take place that actually pushed the earth up. We called it ‘heaving.’ ‘Heaving’ was so bad in that area that it pushed huge pumps and the sump right out of the ground. Eventually, we dug out the sump and relocated it to another area.

Occidental had us dig out the old area, but we never reached uncontaminated earth. Consequently we dumped tons of lime in the hole and covered it up. Every time it rained, pH meters in the freshwater ditches would go off, triggering red flashing lights. All the water in those ditches eventually flows into the Suwannee River. These incidents happened all over the complex.

At the south loading area, a few steps away from the office, ‘heaving’ is the worst I have ever seen at the complex. It was so bad that railroad tracks were often snapped, twisted and bent. We had rail-car accidents because heaving twisted or bent the rails. Overhead, ten-inch I-beams are bent and twisted. When the ground heaved the wrong way, acid drained away from the sump area, spilled over, ate through the walls and spilled onto the ground.

They called in contractors to clean up the contaminated soil. They dug down six feet in the ground, and syrupy, black acid still oozed from the earth.

I mentioned the rail-car wash, early on. This area was a constant source of exposure to toxic pollution: Sulfur dioxide/trioxide, hydrogen sulfide, and fluorosilicate/fluorine gases. There were two acid-brick lined ditches below the tracks to reclaim the wash. The pond water was kept hot and recycled through a high-pressure pump to wash acid and solids from the tank cars. On cold, still nights the fumes were particularly thick; they would take my breath away. Sometimes the fumes were so thick, they were blinding.

We took the heaters out and used the sump for different purposes. Sulfuric or phosphoric acid overloads, well, we would dump the excess into the sump. With the sulfuric acid, we would turn on all the safety showers and water hoses, because a violent chemical reaction was in the making.

The first safety tip ever given me was in 1979 when a fellow said, ‘Don’t step in puddles because they might not be water. After two months and two pairs of shoes, I determined that he was dead serious.

We also used to open sulphur car dome lids in the rail-car wash area. I was looking at a copy of a memo I wrote in June of 1985. I requested, in the interest of safety and productivity, that the rail-car wash be moved to a more remote location on the complex. My manager, at the time, was less than impressed and became angry after I wrote a rebuttal to his response. I saw the reality of the situation, and he did not. I think a comment I made in my rebuttal best indicates the situation: “In all candor, usually the fumes are so bad that the offices have to be evacuated anyway when the tops are being opened.” A year later when new management came to the complex, the new superintendent asked me to resubmit the plan. I did, and it was implemented. All I ever wanted was a safer and more productive workplace.

Starting with the first day we unloaded sulfur at the Swift Creek Chemical Complex, steam coils in the launders overheated. As we unloaded the molten sulfur, it ignited and set the whole place on fire. Back then we didn’t have running water and fire departments from surrounding communities responded. There were no safety showers or places to change our clothes.

Sulfur dioxide and sweat produce sulfuric acid. After I would go home and take my clothes off, I had rashes around my arm pits, knees and thighs.

Leaks from sulfuric acid plants engulfed us in clouds of sulfur dioxide. On days when the sulfuric acid plants were being maintained and repaired, they vented the sulfur dioxide directly into the air. We cautioned our people to stay inside and out of the smoke as much as possible.

In 1983, I took a shift supervisor position in the phosphoric acid evaporation and purification area. All I can say is that was the worst assignment of my working career. I had only two days training before starting work. Personally, I would not call it training. It was a supervisor harping about how screwed up the department was and how happy he was to be leaving. I came away from those sessions knowing absolutely nothing about phosphoric acid production.

Like many others in the evaporation/purification area, I seemed to stay sick all the time. We lived in acidic fumes pouring off the hot acids. So many of us developed respiratory infections, many of the workers thought it was some virus in the air. They went around the plant armed with cans of disinfectant spraying telephones, walls and air-conditioning ducts. During that year I developed some serious ear infections, a near constant upper respiratory tract infection and sebaceous cysts that had to be removed from my hand.

One of the workers told me that the pollution scrubber was shut down on the west side of the filter building. During the year I worked at the phosphoric acid plant, I never saw anyone attempt to put the pollution scrubber into operation.

The Florida Department of Environmental Protection notifies the management prior to visiting the facility to do stack tests for pollution emissions. They had a crew of mechanics remove spray bars and drag them out onto the street. We had to beat the pipes with nine pound sledge hammers to break the solids lose. It was also common practice to pull the scrubber pad on the street and have trucks run over them to break the solidified fluorosilicates lose. All the nozzles were plugged and had to be cleaned or replaced. Nothing could have passed through them. We managed to get the pollution scrubber operational by the time inspectors showed up.

We also made Synspar, synthetic cryolite. Pond water containing about 12,000-15,000 parts per million of fluorine is mixed with hydrated lime and a polymer (flocculent). The water is spun off in a gigantic centrifuge. The Synspar paste was placed in aging tanks. Synspar attaches itself to impurities in the phosphoric acid and is strained out through large membranes covering tanks. It was common for lime reactors to overflow and flood the streets.

Walking through the area I was responsible for was a sickening experience. On the filter decks, six Volkswagen size drum filters churn, suck and spew hot acid. Stepping in front of one of the filters to see if it is binding over, I was often sprayed with a hot acid mist. Passing the hot wells venting fluorine gases, sulfur dioxide and God know what else, kept me coughing and congested all the time. Everything in the evaporation/purification area emits toxic acidic vapors. That was the worst year of my life.

As a first line supervisor, I was required to be a member of the fire fighting brigade. 1983, I became a volunteer Emergency Medical Technician for Occidental. The program was very popular at Occidental because, it was rumored, the insurance company reduced rates. I was dropped from the program in 1994 for diminished lung capacity and high blood pressure.

The problems started in 1985 when an oil line ruptured and began spraying into a turbine blower. For several weeks after the fire, my lungs burned and my throat was raw from coughing. An electrician who was called into repair damage said that wiring had burned off an automatic valve causing it to remain open and saturate the atmosphere with sulfur dioxide.

We were instructed to use sulfur dioxide canisters attached to full face respirators when fighting fires on the sulfur pad. However, the canisters were clearly marked not for fighting fires.

For a number of years, I also used to ride ‘the stack once every working shift with my process water operator. The gypsum stacks on the east end of the property have the appearance of a mountain range. There must be hundreds of millions of tons radioactive gyp-wastes there. When they did a hair analysis on me for radium exposure, I was pretty hot according to the test results.

There are many other toxic materials in those gyp-stacks like lead, arsenic, aluminum, fluorides and by-products from sulfuric acid production. We used to toss most anything we wanted to get rid of in the evaporation ponds atop those gyp-stacks.

When I worked with Gary Pittman, he used to take a chicken leg from his lunch and set it in the pond water. The water was so acidic, the next day, Gary would pull out a bleached bone.

I recall two separate occasions when my Jeep and other vehicles were heavily damaged by fluorine emissions from the phosphoric acid plant. Being naive and unaware of the serious ramifications of the first incident, I casually stated at a meeting that my Jeep had white spots all over it and the windshield looked like frosted glass. My supervisor hushed me up and hurried me out of the room, saying, there had been a scrubber failure. He said that people who had damage to their vehicles should contact security and fill out a damage claim. I was told not to discuss the incident with anyone, but someone did a poor job of keeping the secret. Rumor had it that over $40,000 was paid out.

Occidental got a little smarter after the next scrubber failure. They had the insurance adjuster come out and offer everyone $200 on the spot to have their vehicle buffed. I had two estimates, both body men said that buffing wouldn’t work because the damage was too deep.

Since the collapse of the Soviet Union, and even more especially since Occidental sold the complex to Potash Corporation of Saskatchewan (PCS), the focus of shipping has dramatically changed. They load more single rail-cars than unit trains. We loaded 750 tons on a unit train whereas we only load 98 tons on a single car. The margin of error is greater, more overfills, more dumping of phosphoric acid into sumps and more exposure to toxic fumes.

Standing in the shipping office looking south, there is a mountain of wet phosphate a few hundred yards away. I don’t know the whole procedure, but phosphate is floated out of the dirt with fatty acids, sulfuric acid and ammonia. The phosphate is moved to the evaporation plant via overhead conveyor belts. It was always dripping whitish liquid. These droppings would ruin the paint job on a car and etch the windshield glass which was often replaced.

During my career at Occidental, I was always safety conscious and received many commendations from management. I was requested to write the manual and direct a safety video on unloading sulphur cars. However, I really didn’t understand the nature of other substances to which we were being exposed every day and the mixed exposures. The U.S. Centers for Disease Control put out a National Occupational Research Agenda bulletin in 1998 titled Mixed Exposures. It said, Research has shown that physiologic interactions from some mixed chemicals can lead to an increase in the severity of the harmful effect. For example, exposure to noise and the solvent toluene results in two to three-times-higher risk of hearing loss than either component alone . . . to evaluate possible synergistic effects, laboratory studies of physiologic interactions at the target organs are needed, as are improved animal models for extrapolation to humans.

In my case, I was exposed primarily to sulphates and sulfites, but there were also numerous contaminants in the air like fluorosilicates, fluorine gases, phosphates and the other chemicals related to phosphoric acid production. In addition to many physical problems I have developed, my immune system does not work properly, and it hasn’t for some time.

The emergency medical teams at the complex were required to take hepatitis B immunization. A test was done on me to see if the immunization was taking. The test indicated that I had no immunity after taking the series of shots. The company nurse gave me two more shots, and tests still showed no immunity. At that time she refused to give me any more shots without written orders from my physician.

Staring into the computer screen, writing this, I know that people can only see who I was. In this room, my room, the walls and display cases drip with American Indian artifacts. I ‘ve walked, dived and dug for them. I have open water and cave diving certification. One wall is filled with framed maps and money from Australia, Belize, Norway, Turkey, Israel, Mexico, Guatemala, and Egypt. On another wall is rattlesnake hides. I used to catch them and drown them in water so there would be no holes marring the skins.

My most prized possessions are on my Israel wall: A Jewish flag given to me by an eight-year-old girl, the shoulder patch and rank insignia of a Patriot Missile soldier, Sergeant Randy Rankin, cut from his sleeve the night the war ended. Mike Norris and I joined the volunteers for Israel during the Gulf War. We paid our own way over and used one month vacation time.

Along with a Jewish fireman, Lt. Dan Felton, from Miramar Beach, we made history being the only Volunteers for Israel ever (at our insistence) to be assigned to a war zone. Mike and I were also the only Gentiles there. We spent three weeks with the Tel Aviv fire department. I have a home there. This was affirmed when we went back to Israel to be honored for our service. Commendations signed by General Davidi and Aaron Eshel (the fire chief) also hang on my Israel wall. I ate at Eshel’s house and visited his community bomb shelter.

Now, I know those days are over. I know that if I go out and mow the lawn, I am going to suffer for it. Diving is out of the question. I’m just not the person I used to be, and it’s kind of hard to adjust to that.

*********************

The primary pollutants Jesse Nash was exposed to were sulphur products, byproducts, fluorosilicates and radionuclides. In Patty’s Industrial Hygiene and Toxicology, Vol. 2. 1993, sulfur oxides are noted as having a major impact on the quality of life. Nash was routinely exposed to levels of sulfur dioxide as high as 1280 parts per million (ppm) and possibly even higher (these are considered lethal doses). 400 to 500 ppm exposure are rated as an immediate danger to life. According to government standards 100 ppm can only be tolerated for about one hour before injury occurs, and 20ppm can cause chronic respiratory symptoms.

Page 810, Patty’s Industrial Hygiene and Toxicology, Sulfur dioxide may also act as a cancer promoter. The mortality of arsenic smelter workers exposed to 1ppm or more was higher when they had also been exposed to sulfur dioxide (ref. 93). Additionally, rats exposed to 3.5-10 ppm of sulfur dioxide developed squamous cell carcinomas from inhalation of benzol [a]pryene, but neither compound alone produced carcinomas under the condition of this experiment (ref. 94). Jesse had a basil cell carcinoma removed from his face in 1996.

Hydrogen sulfide is extremely toxic to humans. Several case studies noted neuropsychological dysfunctions that were characterized by impairment of memory, psychomotor, and perceptual abilities in individuals exposed to hydrogen sulfide. Also, heart and respiratory problems have been detected.

Jesse Nash suffers with nearly every adverse health effect associated with exposure to sulfur oxides and hydrogen sulfide. He was exposed to numerous toxic chemicals and toxic metals. Occidental Chemical Corporation and the law firm of Holland and Knight claim that none of the toxic substances could have caused Jesse Nash’s condition. However, Nash’s medical records read like textbook cases of chemical poisoning.

All the accounts by the men in this compilation clearly show that they were exposed to toxic chemicals during their careers at Occidental. Each also exhibits classic symptoms of chemical poisoning.

WIVES ARE VICTIMS TOO

Joann Nash

Dear George,

My name is Jo Ann. I have been married to Jesse Nash for almost 34 years. We have been through a lot during those years, mostly good and of course some bad.

Jesse is a very special person, and I am so grateful that we have each other. We are so very different, and yet, we know each other’s thoughts. Back in June of 1996, after we finally found that Jesse’s health problems were caused by chemical poisoning, and he had used all his vacation time. Jesse called Occidental/PCS. He told them what we had discovered. They told him to go out to the plant for a meeting with the human resources people. The meeting was held in a conference room where the group had been eating watermelon. They never bothered cleaning the mess from the conference room table where they sat and discussed Jesse’s problem. I couldn’t believe it. Jesse was so sure that the company was going to take care of him and help him get the proper treatment. All the offered him was unpaid medical leave.

Jesse worked for Occidental/PCS for almost eighteen years when he had to take medical leave; that was 22 months ago. He had taken out a disability insurance when he was promoted to supervisor. He wanted to make sure that his family was taken care of in case of an accident or illness. We are still waiting for our first check.

I used to own and operate the Nash Quail Farm. I started raising Bobwhite Quail back in 1984. I found that I had developed an allergy to the birds’ dust, feathers and feed. I was taking allergy shots every four days. In June of 1997, I had to give up my business. Since then, I haven’t had any luck in finding steady employment. I am fifty-four years old and work part-time as an independent contractor demonstrating goods in grocery stores, 2-3 days a month.

Jesse had always worked and supported his family. Now that he is unable to work, he has been under unbelievable stress because of our financial situation, and he feels useless and inadequate. If he had not been the “macho type,” maybe things would be easier; I don’t really know.

If he does any activity, Jesse pays the price. His joints swell. Every morning when he wakes up, his right eye is so swollen, its shut. Jesse can only see a little out of his left eye. Sometimes, his face is swollen all day, and other days, he is normal after a few hours. He suffers with headaches and chronic fatigue all the time. We used to be so grateful that Occidental/PCS provided him with a good paying job. Now, I wish he had never gone to work there.

Our two children are grown, but our daughter moved back in with us in the summer of 1996. She had become ill with fibromyalgia and chronic fatigue syndrome. He immune system is very poor. She and her husband were divorced because he could not deal with her illness; he has never had a headache.

I am not sure what caused Jessica’s illness, but sometimes I wonder. I wonder about the residue Jesse brought home on his ski and clothes. Jessica was always wearing one of his work jackets when she was a teenager. After she was married, she would wear his jacket when visiting us during cold weather. The sad part is that Jesse and Jessica were to caring and fun loving people. They were energetic and intelligent people. They’re not like that anymore. All three of us suffer from short term memory loss.

These days, I do most of the driving because it is unnerving for Jesse. He gets embarrassed because his memory is getting worse, and he worries about what is going to happen next.

We looked forward to his retiring at 65 and planned on traveling. Now, I worry about the mortgage payment, buying groceries and paying the bills.

Thank God. Jesse was approved for his Social Security disability, last year. When the first check arrived, we were so happy. It gave us hope, and we knew that ITT-Hartford would come through with disability insurance, but we are still waiting.

Presently, we are in trouble with our credit cards because we had to live off them for a while. I kept borrowing money every month to pay the credit card bills, and finally, I realized that had to stop.

We went to workman’s compensation mediation in September of 1998, but it was continued until December. I want to pay the credit cards off, but I can’t do that until Jesse is paid his disability insurance or workman’s compensation.

I know we shouldn’t complain, there are people who have more problems, but some days I wonder if I can keep enduring the feeling of shame and bewilderment.

We are still waiting for resolution, and Jesse has received no medical treatment for his health problems.

Our daughter and son live on our property. Jessica has married to young man she met at a support group meeting.

Thank God for family.

Jo Ann Nash

Charlotte Baldwin

In May of 1993, Billy was laid off from Occidental Chemical Corporation. In August, he was called back to work, and in September, the first symptoms of leukemia appeared.

Billy has always been the type of person who is up early in the morning and goes to bed around eleven. But in September, during a plant overhaul, Billy was working ten hour shifts. He would come home and go right to bed. This went on for several weeks until I finally became worried and asked him if everything was all right. Billy said that he felt tired all the time.

Being tired all the time was strange for Billy. He was sick at his stomach, had headaches and was white as a ghost. I tried to talk him into going to a doctor, but he told me that if he took time off from work he would lose his job.

When I came home from work, Saturday, November 13, Billy said that he couldn’t take it anymore, he needed to see a doctor. I rushed him to the emergency room where he was immediately admitted for severe anemia and stayed there for three days. The doctors at Lakeshore Hospital in Lake City, Florida ran a blood test and bone marrow biopsy. They said they could not find anything wrong with Billy.

Billy’s doctor prescribed of vitamin B12 and folic acid once a day for a year. When I went to have the prescription for B12 filled, the pharmacist immediately asked who wrote the prescription. Then I asked what was wrong, and the pharmacist said that athletes didn’t take that much vitamin B12, and he would have to verify the prescription with the doctor.

After two weeks on B12, Billy was not getting any better. His white blood cell count was rising. We were told to see Dr. Vernon Montoya in Gainesville, Florida. The doctor examined him and had blood drawn. After waiting several hours, Dr. Montoya called us in and he asked Billy how he managed to walk into the office with such a low red blood cell count.

Dr. Montoya told me to take Billy to North Florida Hospital and be admitted. They gave him a transfusion of three units of blood, and they did a bone marrow biopsy. Dr. Montoya told us the results would take a few days, but he never told us what he suspected. A few days later, the phone rang and I answered it. The nurse asked to speak with Mr. Baldwin, so I handed Billy the telephone.

Dr. Montoya told him to come to his office at nine the next morning because they needed to talk. Upon hearing Billy make the appointment, I took the telephone and asked what was wrong. Dr. Montoya said we would discuss the situation in the morning. I was worried and persuaded the doctor to tell me what was wrong with Billy. Reluctantly, Dr. Montoya told me that he had the leukemia, the worst type, AML. It broke my heart, but I never told Billy. I waited for the doctor to tell Billy because I could not bear to tell him such bad news.

Somehow, I didn’t want to believe this was happening to us, but when we went to Dr. Montoya’s office, he said that if Billy didn’t get help soon, it would be too late. I don’t think that anyone can imagine what those words did to us. Billy had always been healthy and robust. He liked to work around the house, raise chickens, fish, hunt and do things with our children. With those words knew those days were over, maybe forever.

We discussed treatments and Dr. Montoya said Billy could get better, but he needed to go to Shands Hospital in Gainesville, Florida where they specialized in treating cancers. Dr. Montoya proceeded to call Shands where Billy was admitted for chemotherapy on December 27, 1993.

For two years after that day, our lives became a living hell. I was also working for a nursing home in the dietary department. I had to clock-in at five in the morning and work till one in the afternoon. Then I went home, tossed a load of laundry in the machine, fed the chickens and dog, took a shower, and drove about forty-five miles to Shands. I would stay until eight or nine at night, go home, finish the laundry, get a few hours sleep, get up at three-thirty in the morning and do it all over again the next day. On weekends, I would stay at Shands with Billy, we would walk from one end of the hospital to the other pushing his I.V. It was like that, off and on again, for almost three years.

Billy improved, so they let him come home on January 25, 1994 for a few weeks. When we went to the doctor for a checkup, his white blood cell count was very high. This meant the first round of chemotherapy didn’t work. Billy had to go back to Shands for a second round of chemotherapy. The nurses called it the “kick ass” treatment. Believe me that is exactly what it was. The treatment made Billy so sick, it was unreal. His fevers were so high that they had to pack Billy in ice. This is when I became a nurse without a license. I had to learn how to change the dressings, draw blood from the I.V. line, give injections, and everything else that went along with home health care. After the first few months, I knew more about blood cells than most doctors. I caught on quick, but that was only the beginning.

Many times, I remember leaving the hospital at night and cried all the way from Gainesville to Lake City, because there was nothing I could do to help Billy. I felt totally helpless.

After thirty-three days, Billy came home from Shands, and for once, I thought things were going to get better. But when Billy was going through the second round of chemotherapy, the doctors began talking about the possibility of a bone marrow transplant. At first, Billy didn’t want to have a bone marrow transplant done. Then he asked me what I thought, and I said that it was his decision.

Billy had befriended a young fellow named Jimmy at Shands. He had six children. Jimmy had leukemia, too and had been through the routine like Billy. He decided against having a bone marrow transplant. Jimmy’s leukemia remission didn’t last, and he never left the hospital. That is what changed Billy’s mind.

On May of 1994, he went back to Shands for more chemotherapy. He came home for awhile because the leukemia was in remission. He began preparing for a transplant in June. Billy’s older brother’s bone marrow matched, which was very lucky. At that point the doctors began testing him for any problem imaginable to make sure he could undergo the transplant.

They even gave Billy psychological testing. About half way through, he said, “These damned psychological tests are not going to save my life, my brother is.” He never finished the psychological tests.

On June 21, he went into Shands for the transplant, and it was pure hell. His hair fell out again. His mouth turned inside-out. He couldn’t talk because a chunk of flesh was hanging out of his mouth. All Billy could do was point to what he wanted. Aside from being depressing, I think I was more frustrated because there was nothing I could do to make things easier for Billy.

Billy was at Shands for eight long weeks. He had to wash out of a pan with sterile water. His only exercise was riding a stationary bicycle and there was no space to move about in his room.

I walked into the room one morning and he was covered from head to toe with a rash. I became worried and asked the doctor what was wrong. The doctor said that it was “graft versus host disease,” which meant his body was rejecting the other bone marrow transplant. I thought, “what’s going to happen next?”

The doctors began give Billy high doses of steroids. His mouth was still swollen, so he couldn’t eat, so they had fed him intravenously. They called it his meat and potatoes. He also had a bag of white stuff that looked like shortening to supplement his fats.

One day, he began complaining of headaches. Later in the evening, the headaches became so bad that I stayed with him later than usual. I left the hospital about ten that evening. About two in the morning, the telephone rang. Upon waking, I knew it was about Billy and thought. It was his doctor. He said that Billy had a seizure and his brain was swelling. Getting dressed, I could only wonder if things could be any worse.

By the time I arrived at the hospital, he had lost his eyesight. They said it was temporary and caused by the seizure. But nurses were staying with Billy around the clock. All I remember was being totally exhausted. The next thing I remembered was waking up in the chair beside his bed.

After a few days, the swelling began to subside. Everything seemed to be slowing down. We had a few good days, and the doctors said Billy would be able to go home soon. His red blood cell count was rising, and we thought everything was going to be all right. Then he contracted a CMV virus. The virus had to be treated or it would have killed Billy. Again we were devastated. It seemed we were back to square one and starting all over again.

Again the doctors started Billy on I.V. medications. His blood count went up and down like a roller coaster for the next few days, and the fevers would come and go. I often wondered if we were going to make it through the ordeal. Every day brought something new, different and most often disturbing.

Finally, Billy was going to come home, but it was only out of the hospital to transplant housing facility. We had to be within five minutes of the hospital in case something went wrong. I had to draw blood every morning and take it to the hospital. They ran tests to see if Billy needed red blood platelets. The Home Health people taught me how to hook up I.V.’s and flush the lines. Billy had to learn how to walk and hold a spoon without shaking. He had to hold onto the wall to take a shower while I bathed him.

Billy came home at the end of November. Our youngest daughter, Stacy, was about to be married in January of 1995. Billy was supposed to walk her down the isle. Fortunately we got a break. He didn’t have to be hooked up to I.V.’s on the weekend, and Stacy was going to be married on Saturday. Billy was going to have to wear a mask with his tuxedo, but Stacy didn’t mind as long as her father was at her side. He never got to walk Stacy down the isle. He was back in the hospital with pneumonia, another two weeks at Shands. It seemed like we were permanent fixtures at Shands. I knew the layout better than I knew my own house.

Billy came back home again to home health care. He began to lose weight. The graft versus host disease (GVH) has spread to his digestive tract. He told the doctors, but they dismissed his complaints. Billy was so malnourished and skinny; I could count his ribs. I became fed up and took him back to Shands. The doctors finally listened to us, did some tests and found that the GVH had spread to Billy’s digestive system. They put a feeding tube through his nostril, down the back of Billy’s throat and into his stomach. Again I was learning something new to do with my spare time.

After that ordeal, it seemed like everything was smoothing out. Billy was still on drugs, but life seemed to normalize somewhat. By 1996, Billy finally came off the drugs: what a great day! No more I.V.’s, lines to flush, dressings to change and no more pills. Today, Billy is in remission. Although we have had some minor problems, my Billy is all right for now. I hope he stays that way for a long time.

Note: Potash Corporation of Saskatchewan, the corporation that bought out Occidental is presently building another chemical complex not a quarter-mile from Charlotte and Billy Baldwin’s home.

Reba Vann

Dear George,

I am going to tell you my story about how Clinton and I feel about this whole thing.

We were married in 1966 and have two children. Our life was normal. We were always going places and doing something. Sometimes, twice a year, we traveled to the mountains. We dreamed about buying a small place there when the children were grown. Our son graduated from high school in 1984, and we thought that would be our chance.

In 1983, Clinton went to the doctor and was told his liver enzyme levels were out of range. That news halted everything; our world was put on hold. When the people at Occidental Chemical saw the report, they put Clinton in another department away from the chemicals.

In 1984, he had to have a liver biopsy that revealed toxic problems. At that time, he was still in another department. Becoming worried, Occidental sent the test results to their doctor in Niagra Falls, New York for review. He said there was nothing to be alarmed about and something else had caused Clinton’s problems. They sent him back to the laboratory. The doctor then wrote the supervisors to hush up the incident (we have hand written letters confirming the incident).

While Clinton was still under doctors’ care in 1984, we took a trip to the mountains. We met a man who had some property to sell. It was almost straight up the side of a mountain, and Clinton walked up without any problems. By 1988, he began to be tired all the time. He had trouble getting up in the morning. Clinton would have to set the alarm clock for four-thirty in the morning to be at work by seven. It took him at least an hour-and-a-half to get out of bed. It wasn’t laziness; he didn’t have any energy. He began to fall about this time; he could be standing still and fall.

Our son married in 1988 and our granddaughter was born in 1992. Clinton has never played with her, or cuddled her when she was crying, because he can’t. This is heartbreaking for Clinton, and our granddaughter wonders why her grand daddy can’t romp around on the floor with her.

In 1989, I became ill and finally had a heart attack, and now, I am also disabled.

In 1990, Clinton went to my doctor in Gainesville who diagnosed him with muscular dystrophy. We believed the diagnosis until we discovered that Gary Pittman was diagnosed with the same symptoms including muscle weakness, no energy and irregular heart beat. All the symptoms were identical.

We began to think about the similarity of symptoms in 1993 when both Clinton and Gary were out of work. I went to our small library and picked up a book about toxic chemicals. All the chemicals and symptoms Clinton and Gary had were cited in the book. Occidental had to have known that they were poisoning those people, the information was common knowledge to people in that business.

Later, we went to a lawyer who seemed very interested and took our cases. Other lawyers in the area advised him not to take our cases, so he backed off. After we hired a workman’s compensation lawyer in Ocala, he wanted back into the picture and filed our case on February 27, 1997, before he thought our four-year statute of limitation ran out. Our case went to Federal court and was not denied; the judge must have thought the suite had merit. When the case went to Federal court, the lawyer dropped us like hot potatoes. We were left out of the Coker/Boyer toxic tort law suit. They said we couldn’t join until the case was released from Federal court and when it was cleared up, we could join in the law suit.

Here we are, two years later, and they have told us three different stories as to why we can’t join in the law suit. At the time, we were upset and depressed, but it doesn’t matter now, because I think, in the end, all involved will have to answer for what they have done to others (including Boyer/Coker and Ferro).

People I have talked with act caring, but unless something like this happens in your family or friends, it’s impossible to know the heartache and worry. The worst part is that family and friends we thought cared never call to see how things are going.

As for myself and Clinton, we take things one day at a time. Most days are spent sitting around the house. Clinton is too tired, hurts all over, or has bad headaches to do anything. Sometimes, he can’t remember what he did or where he put something five minutes ago. Occidental/PCS owe the people they made ill. The worst part is that many of those people who worked for Occidental have no idea what made them sick, or their families don’t know what killed their loved ones. I know their lives are as bad or worse than ours.

At times, it is very depressing to see someone I loved and cared about for thirty-four years sickly. The most depressing part is that there is nothing I can do to make Clinton’s life any better. I hope this letter will help you (and us), and we greatly appreciate all that you have done.

Hope to meet you soon.

Good Bless you,

Reba Van

Gloria Pittman

Sometimes, it is very difficult living with Gary. He has mood swings and lapses into depression because of his health problems. He also has memory loss because of being poisoned by chemicals at Occidental Chemical Corporation. He will lay something down and forget where it is. Then he will accuse me of misplacing his things. He has fallen and hurt himself many times. He stumbles and bruises himself. On Christmas morning, one year, he fell and knocked one of his front teeth out. I contend with all the problems hour by hour because I love Gary. I know that it is not his fault.

When I first met Gary Pittman, he was so full of life. He had many friends, and people loved to be around him. I loved being around Gary. Whenever he called, I always made the time to see him. We fell in love. We had dreams and bright hopes for the future. Two years later we were married and started a family.

After we were married, we moved onto a piece of land on his father’s farm. It was nothing more than a plowed field. Gary would work at the chemical plant all day, come home and work around the house. Even on his days off, Gary was always working in the yard, planting trees, grass and leveling the land. He always had a fine vegetable garden, tilled and tended with hand tools. He was always on the go. Gary was healthy, felt good and the hardest working person I ever met.

Before long we had a beautiful home and our first born, a daughter, Scarlett. We were a family. It seemed like we always did fun things together: listened to music, barbecued food and lounged around in the hot tub that Gary installed. About that time, his oldest daughter, Nicole, from a previous marriage came to live with us. We enjoyed each other and enjoyed life. Gary was a good husband, father and provided good life for his family.

It wasn’t long before strange things began happening to Gary. In 1986, he developed a nasty rash. Large, round, red circles covered his back, arms and hands. The rash seemed to crawl from his back onto his stomach. The itching was intolerable, and he would ask me to rub lotion on him. Finally, the rash became so bad that I thought Gary was going to be scarred. I told him that he needed to see a doctor. Fortunately, there was a doctor living down the road from us, and Gary called him.

Upon checking the rash, the doctor said that he didn’t know the cause, but it looked like an allergic reaction or mycotic infection. He prescribed some lotion and medication which helped. The rash cleared up.

Shortly after that episode, Gary’s right hand became swollen and very painful. Again, he went to the doctor. They did X-rays of his hand and said it was a hairline fracture. This was strange because Gary didn’t remember doing anything to hurt his hand. We both brushed the incident off and forgot about it.

About 1989, we bought a house on the golf course. The price was right, and the home was perfect for a growing family. Brittany, our second daughter, was born shortly after we were settled in our new home. We lived on the number three fairway and times were good for us. Gary always got good performance evaluations at Occidental which meant pay raises and promotions.

We had wonderful times together as a family, but they didn’t last. In 1991, Gary became very weak and fatigued; he lost about twenty pounds and looked drained. We didn’t know what was wrong. He finally went to the doctor, he ran tests, but couldn’t find anything. The doctor thought the problem might be Lyme’s disease, but tests were negative. Being at a loss, he prescribed antibiotics.

After two weeks off from work, he began to feel better. We went out and bought new pants for work because he had lost so much weight. Still not felling well, Gary went back to work because he was afraid he would lose his job at Occidental. After returning to work, his health seemed to improve, Gary never seemed the same after that. He was always tired. Worried about his health, I would tell him not to push, but he never listened to me.

I would wake up around five in the morning and make his lunch, giving Gary an extra twenty minutes to sleep. Every morning, he would say, “I would give a hundred dollars for some more rest.” He seemed so tired, but Gary kept on working. He was loyal to Occidental and dutifully went to work every day.

February 9, 1993, Gary came home from work early. He was sick, vomiting for about half hour and had an unbearable headache. Later that night, he was coughing up blood. He thought it was a virus, but no one else in the family any symptoms.

The next morning, I went into labor with our third child. Still, sick, poor Gary had to take me to the hospital. While I was giving birth to James, Gary was trying to survive in the waiting room. When he came in to see me and James, he looked like death. He didn’t want to go home, but I told him I would be all right. I was worried that he wouldn’t be able to make it to the house.

He took vacation time because of the birth of our James and his sickness. After several weeks off from work, he felt better and went back to work. Three months later, Gary came straight home from work and went to bed, and that is where the nightmare began for me. He said his lower legs and feet were killing him. The next morning, he called the foot doctor. The doctor referred him to a regular medical doctor because something else was causing the foot problems. The medical doctor did blood tests and an E.K.G. He told Gary that he had a heart attack but it was some time ago because the scar was old. That news almost killed me. I was afraid and apprehensive for our family. We had four children, and I didn’t know if they would have a daddy, or I would have a husband much longer.

Two days later, his legs were still hurting, and he was also having chest pains. I wasted no time in taking him to the emergency room. There, they monitored his heart and did more blood tests. After several hours, the doctor came out and told me that Gary’s C.P.K., isoenzyme levels were off the scale. The level was over 5,000 and normal was between 100-200. Gary was given a medication for the pain. Then we were told to see our regular doctor as soon as possible.

Our doctor said that Gary had a muscle destructive process and there was nothing he could do except refer him to a specialist. We went to the specialist with medical records in hand. After reviewing Gary’s blood test results, the specialist said that a muscle biopsy had to be done the same day. He said we couldn’t wait because Gary was on the verge of death. The results indicated that Gary had autoimmune disease, polymytosites (simultaneous inflammation of many muscles), and that the blood tests proved the diagnosis. The doctor said that if he could get the C.P.K. down, he could get the muscle disease under control. The only problem was that Gary would never be the same.

We were both in a state of shock from that news. Gary was so; he could barely sit up for his medications. Afterwards, he would lay back down on the sofa. Fortunately, the girls were at school during the day. It was James, Gary and me at home. At times, the pain became so intolerable, he could not stand the slightest aggravation. I would have to take James into a bedroom and watch television and play. This was a very sad and lonely time for me and the children.

At first, we went to the doctors about every six weeks. Every time we talked with the doctor, he told us something else was wrong with Gary. One doctor said that Gary had emphysema, but not to worry. If he couldn’t get the muscle disease under control, Gary wouldn’t live long enough for the emphysema to kill him. After visits like that, I felt like we had gone to hell. The ride home was quiet and seemed like an eternity, but somehow, we always felt like things would get better. The doctor said Gary was suffering with nonspecific myopathy, polyarthritis, chronic obstructive pulmonary disease, irregular heart beat, and high blood pressure, and he was only thirty-nine years old.

In 1995, we decided to ask for a second opinion and I took Gary to Tifton, Georgia and consulted with another specialist. All the doctor told us was that Gary had myopathy (muscle disease) and suggested we go to Duke University if possible. If we could not afford to go to Duke, the doctor suggested that Gary keep seeing the same doctor. Having proper tests done at Duke University was too expensive, and we had the children to worry about.

Later, the doctor in Gainesville told Gary that he had reached the “maximum medical improvement” and suggested he talk to the company about going back to work. However, the doctor did not give him a medical release to go back to work. Gary went and spoke with the human resources director about returning to work in some capacity. He was told flatly that he could not return to work in his condition and taking the medications that had been prescribed.

Gary’s doctor in Valdosta, Georgia did chest X-rays and pulmonary breathing tests. The X-rays showed blisters on his lungs with some fibrotic changes. The lung doctor told him that his lungs were very bad for a thirty-nine old man. He then asked Gary where he worked and what they made. Gary told the doctor about the fumes and chemicals he worked around. The doctor said that Gary’s condition had to be work related and put it in the report. Gary asked him not to enter the information on the medical report because he intended to go back to work. The doctor told us that he had to include Gary’s condition in the report because it was true.

Then Gary went back to the cardiologist and told him what the respiratory doctor said, but he avoided talking about his lung problems. The most interesting aspect of our visits to the doctors was that when we brought up the possibility of chemical poisoning, none of them wanted to discuss the subject. One doctor even told us, “You don’t want to go there.” He would become very nervous every time we mentioned the potential of chemical poisoning.

Another doctor even told Gary that he would be blackballed from the industry, and he would never get a job anywhere. Gary was unable to work anyway, so it didn’t matter.

Finally, we filed a toxic tort lawsuit against Occidental. Gary was very depressed at that time. He didn’t want to sue Occidental. He was deeply hurt to realize that the company he loved and put the better of twenty years had poisoned him. He would tell me over and over that we had to do something to help the others. Gary wanted to help those people who didn’t know what was happening to them.

Gary became so depressed, he started to see a psychiatrist. He thought it might help to talk to someone who could help, a professional. The psychiatrist diagnosed him with “reactive depression and prescribed antidepressants. Gary often became so depressed, he told me he wanted to die because he had so many problems. I always told him that he couldn’t die because I needed a husband and the children needed a daddy.

Of course, there were money problems. Gary was drawing 60% of his wages from a long-term disability insurance policy. We had to sell our home on the golf course, move back on the farm and start all over again.

There were times when his feet and lower legs would swell so bad, Gary would be bedridden for weeks at a time. The pain was intolerable. I remember hearing him talk to himself late at night and the early morning. The only way he could go to the bathroom was to drag himself across the floor. When he was that bad off, I would load the wheelchair into the car. I would get Gary’s seventy-three year old father, and we would carry him to the car. We would drive to Gainesville where I would help him into the wheelchair, push him into the doctor’s office. They would give Gary steroids and pain killers. By the time we arrived at the doctor’s office, Gary would tell me that his feet were so swollen, he couldn’t feel the pain anymore. Sometimes, it looked like his feet were about to rot off.

By 1996, we had done extensive research on the chemicals used at Occidental and what they did to the body. We learned that Gary’s symptoms and health problems were identical to those stated in the books, but we needed proof. We found a doctor in Dallas, Texas that specialized in industrial toxicology. Wasting no time, we contacted a coworker who had the same health problems as Gary and with his wife we drove to Dallas.

The doctor reviewed all Gary’s medical records then took blood and hair samples for testing. Next, he underwent a brain spectroanalysis to determine if there was any brain damage. When the results of blood and hair analyses came back, they showed toxic chemicals present. The brain spectroanalysis showed neurotoxic exposure with some brain damage. The diagnosis was “toxic brain syndrome.”

No sooner than we got back from Dallas, Gary had to have cysts removed from his buttocks, twice. Later, he had to have a cyst removed from behind his ear. The doctor said he had blood poisoning.. All of the episodes were very painful.

Gary would have attacks of irregular heartbeat. Every time, it was a trip to the emergency room. We finally requested copies of the readouts so there would be proof. Sometime, the attacks were so bad that he would almost pass out.

We never knew what was going to happen next. I remember one time when Gary’s feet were swelling again. I took James to my mother’s house. When I arrived at my mother’s house, my father told me to hurry home. Gary had fallen and broke one of his toes. Arriving home, I loaded his wheelchair into the car, and got his father to help me carry Gary out. It was another day sitting in the emergency room, and then off to Gainesville for steroids and pain killers.

Gary’s memory was steadily getting worse. He seemed to be doing all right and decided to drive into Live Oak. He wanted to get out and buy some smoked sausage for supper. He was gone much longer than usual. When he got home, he looked a little strange. Gary told me that he got lost and didn’t recognize the surroundings. The incident scared me and Gary because it was just up the road. Another time, he became upset when we were driving to Lake City. He insisted that I pull off the road and wait until he could get his bearings. These episodes last anywhere between five and twenty minutes.

These days, he doesn’t go anywhere alone. I drive Gary everywhere because he feels like the car is still and the road is coming up on him. It gives him an eerie feeling.

We eventually went to another doctor in Tampa for a second opinion. He said that toxic myopathy could not be ruled out because of Gary’s workplace exposure to toxic substances. I believe his whole body has been poisoned and he is lucky to be alive. Both mentally and physically, he was a very strong man. He had to be. Otherwise, Gary would not have survived everything that has happened to him.

These days, we don’t go anywhere except to the doctors’ and lawyers’ offices. I do the errands because Gary is always in pain.

We come from good stock and were raised to do what we think is right regardless of what people think. Most of the people in Hamilton County either work at the phosphate mines or have family working there. It used to be that people would visit us all the time, but since we filed the lawsuit, they don’t come around any more. Sometimes, it seems that people go out of their way to avoid us. This hurts Gary and me because we have known most of those people all our lives. It’s hard on the children, but they support us; they love their daddy.

It took courage to stand up to Occidental, it is a huge corporation. The management at Occidental knew exactly what they were doing to the workers; they were poisoning them. They told the workers that they were breathing “harmless vapors.” I intend to fight them with my body and soul for what they did to my husband and our family. We all intend to see that the next person who goes to work at the mines trying to earn an honest living isn’t poisoned to death.

Karen and Bobby Hobby

Both Karen and Bobby Hobby worked at the Hamilton County, Florida, Occidental Chemical Complexes. On January 23, 1998, Bobby Hobby died of Multiple Myeloma, a bone cancer. About 13,500 people per year develop the cancer and African Americans are 2.5 times as likely to contract the disease than other ethnic groups and males are 1.5 times as likely to develop Myeloma that females. Generally, the cancer affects the older population; however, the recent trend indicated that the younger population is being affected. Professor Brian Durie, said in Myeloma Today, December 1993, “The recent trend toward younger patients in some populations implies that environmental factors are more important in the 1990′s.” Myeloma is a terminal disease.

Karen Hobby

I began working at the occidental Swift Creek Complex in 1987. I met Bobby there, we began to date and were married on February 11, 1989. We had three children, Kevin, Amanda and Nicholas.

I worked at Occidental until 1992 when I was laid-off. I was a helper at the Swift Creek Purification complex doing everything from cleaning to changing filters. Most of the time, the fumes were so bad, the pores on my face felt like they were on fire. We seldom had proper equipment to work with.

We had to change the filters, once a day, handling the acid saturated filters with leather gloves instead of acid resistant rubber gloves. Sometimes, I would ask Bobby to get me rubber gloves because when I asked my supervisor, he would say they were not in the budget.

When I first went to work at Occidental, my hair was a sandy-brown, but before long the acidic fumes caused it to change color. It was a splotched orange to begin with, and I dyed it to match and then it turned green. For a few months I was running around with orange and green hair. I finally wore a hat until my hair went back went back to normal. It was the acid in the air reacting with the hair rinses and coloring that caused the change in colors.

Bobby’s last job at Occidental was doing maintenance at the Suwannee River Complex. He had to maintain and fix equipment in every department. He was a very dedicated employee and never refused overtime. He was called in for emergency repairs at all hours and even on holidays, almost never turned his supervisor down. I remember the last Christmas he worked (1995), he was supposed to have the day off, but they called him and Bobby headed out the door. I said that he needed to be home with me and the children on Christmas. Especially, for the children while they were young.

April 1996, we had an automobile accident. Two weeks later, Bobby’s back began to hurt him. There were times he couldn’t get up, but somehow he continued to work. When Bobby finally went to his primary care doctor, he only found a few slipped disks. Eventually, he went to see a neurologist who found a broken vertebrate. Because of the accident, the neurologist ordered an MRI scan. Still believing the injury was from the accident, he told us to prepare for the worst possible case scenario; it was possible that the vertebrate was broken and needed alignment.

Two weeks later, we went back to the Neurologist. We were not prepared for what he had to say. They had discovered a tumor inside the bone and that is what caused the break. The doctor referred us to a specialist. After the consultation, Bobby was admitted into the hospital for a bone biopsy (this was also the first day of school for the children). They did a battery of tests including a bone biopsy; the diagnosis was Multiple Myeloma. The survival rate was about 2-3 years, and there was no cure.

On September 9, 1996, Bobby underwent surgery to replace the broken vertebrate in his back. There was no guarantee that Bobby would ever walk again because the tumor was directly on his spinal cord. The surgery was supposed to take twelve hours, but it only lasted six. Bobby was in the hospital for one-and-a-half weeks. When he came home, Bobby needed twenty-four hour care. He was in an upper body brace and a wheel chair. He would try to walk some, but it was difficult and very painful for him. I had to bath and take care of him all the time. One time he passed out in the bathroom. That lasted for about six months.

He began radiation treatments before the surgery. Afterwards, they started Bobby on chemotherapy. At first, the treatments were once a month. He was admitted into the hospital for about a week, and after a week at home, Bobby was back in the hospital sick again. The situation was like that until the bone marrow transplant.

Bobby’s transplant donor could only be a brother or sister or self, no anonymous donors. It turned out that his brother and sister were not matches, so the only choice was a self stem cell transplantation. He was given medication to boost his stem cell count, then Bobby spent three days hooked up to a machine to collect his stem cells.

For eight days, he went through heavy chemotherapy, and on the tenth day, they did the transplant. The procedure was new at Shands, and Bobby was the first person undergo the treatment. He stayed at Shands for another week or so. Since we did not live far from the hospital; they let Bobby go home. I took him in for laboratory tests and to receive transfusions, every day.

He continued to see the oncologist once a month for therapy which was supposed to straighten his bones. But on December 27, 1997, Bobby was admitted back into Shands with pneumonia because of heavy chemotherapy after the operation. Two weeks later, he broke his left leg because the cancer had weakened the bone.

Bobby’s bone marrow transplant was not successful, it seemed that the cancer was even more active than before. On January 23, 1998, Bobby lost his battle with cancer. He left behind three children: Kevin, 12, Amanda, 8, and Nicholas, 3, and nine months later we are still trying to pick up the pieces of our lives. Both Kevin and I are in counseling. I hope Amanda will join us soon, and Nicholas, he doesn’t understand why his dad had to leave. Nicholas wakes up crying at night asking for Bobby; he wonders where his dad went.

The holidays will soon be here: Our first Thanksgiving and Christmas without Bobby.

Bobby Hobby

October 24, 1949-January 23, 1998

The following are edited excerpts from Bobby Hobby’s deposition while in the hospital several months before he died. Being on medications and in pain, the attorneys often had to ask questions several times. I have omitted repetitious questions and answers and reworded the dialogue to make it more readable while maintaining the integrity or the deposition.

In the following segment, Hobby

is being questioned about a sulfur dioxide release

and Occidental’s subsequent measures to conceal the accident.

Page 82-96

Attorney: At any point in time while were you were employed with Occidental, were you

aware of any gas leaks.

B. Hobby: Yeah.

Attorney: Approximately when was this?

B. Hobby: (No response.)

Attorney: About ten years ago, fifteen years ago, five years ago?

B. Hobby: (No response.)

Attorney: Was it in the eighties?

B. Hobby: It had to have been in the eighties, but I don’t–

Attorney: Now, were you working days or nights?

B. Hobby: –I don’t remember–

Attorney: I’m sorry, go ahead. You don’t remember?

B. Hobby: –remember the exact an exact time–no.

Attorney: Were you working nights when the gas leak occurred?

B. Hobby: Yeah.

Attorney: How did you know there was a leak of some sort? What led you to believe that

there was a problem at the plant?

B. Hobby: Well that’s when — the next day , some of the vegetation around the — it started

turning — well it started dying, in other words, turning yellow.

Attorney: How did it smell, the plant?

B. Hobby: It stunk.

Attorney: Was it a normal smell that you you’d been used to smelling every single day

you’ve been working?

B. Hobby: No. It smelled like rotten eggs.

Attorney: Was this something that occurred every day?

B. Hobby: This was sudden.

Attorney: After you smelled the smell, how long did it take for the vegetation to start

dying?

B. Hobby: Like, I say — the next day, we could see around in back of the plant was turning

yellowish.

Attorney: How much are we talking about, several acres, several miles?

B. Hobby: A couple of acres.

Attorney: What did you see Occidental do in response to the vegetation dying?

B. Hobby: That’s when they had the laborers come out with a big truck and sprayed the

whole area to kill the grass.

Attorney: What was it sprayed with — you mean like weed killer?

B. Hobby: Oh, some kind of weed killer. I talked with the laborers. I don’t remember the

names, but it’s the same chemicals. The next day, I got some to spray around the

shop to kill the weeds.

Attorney: Did it kill the weeds?

B. Hobby: It killed the weeds.

Attorney: How did they usually get rid of the weeds?

B. Hobby: For that area — they usually mowed it or had the laborers chop them down with

swings.

Attorney: Any other time that you are aware of when they used weed killer in that area — in

mass quantity, such as to cover an acre or more?

B. Hobby: Not to cover the whole back area.

Attorney: Was that the only time?

B. Hobby: Yeah.

Attorney: Anything else get sick back there that you are aware of, Mr. Hobby?

B. Hobby: Animals. Well, the pond in back and the pond in front — all the fish died.

Attorney: Can you describe — please — on the record what the fish looked like?

B. Hobby: Well, the big ones that were still alive — they were blown up; they were gasping

for air. And the ones laying on top dead, they had little sores on them.

Attorney: What did the sores look like?

B. Hobby: Just infested little sores. Little gnashes — you know — opened up wounds.

Attorney: How many fish were there?

B. Hobby: Several hundred.

Attorney: Anything else?

B. Hobby: At that time, no, but a few weeks later they got a bunch of us together on a truck,

and we loaded up some cows.

Attorney: Who told you to load the cows up?

B. Hobby: I suppose it came down from the front office, I don’t know.

Attorney: Did you decide on your own to remove these cows, or was it something you would have been instructed to do?

B. Hobby: I was instructed to do it.

Attorney: What did the cows look like, Mr. Hobby, that you were told to remove?

B. Hobby: They were real skinny and had sores on them.

Attorneys: How many cows are we talking about?

B. Hobby: I know of twenty that were loaded on our truck.

Attorney: Were you raised on a farm?

B. Hobby: Yeah.

Attorney: Do you know what a healthy cow looks like?

B. Hobby: Yeah, definitely. These cows were skinny, poor, and had sores all over them.

Attorney: Mr. Hobby, was this done in broad daylight or was this done the middle of the night?

B. Hobby: The night.

Attorney: Was there ever any discussion with regard to reporting this to third parties or talking about it to anybody else, or not talking about it to anybody else?

B. Hobby: We were just told to load them up, and that was it. The next day was as usual.

Attorney: Did anyone at Occidental ever advise you that it never happened?

B. Hobby; Yeah, but I don’t remember who.

Attorney: My question to you was — well, I’m not saying did they deny that it ever happened, my question to you is did they tell you –

B. Hobby: It didn’t happen. If it ever came up about any cows or anything, no, I knew nothing about it.

Attorney: What kind of salary were you making when you left?

B. Hobby: Good.

Attorney: Were you aware of any other employers in your county or surrounding counties, that paid equal to what Occidental paid for salaries?

B. Hobby: No.

Attorney: What was the drinking water like at Occidental?

B. Hobby: It’s got a bitter taste to it, and it stinks.

Attorney: How would you describe the stink?

B. Hobby: It’s got a bad — bad odor to it.

Attorney: What color was it?

B. Hobby: Sometimes it was brown, real brown.

Attorney: Did you drink it?

B. Hobby: Overall, I drank some of it, but basically, I brought my own water. I couldn’t stand the taste of it.

 … … …

In the following segment, Bobby Hobby describes how Occidental went about

cheating on pollution emissions tests and plant inspections.

Page 111-125

Attorney: Were you ever present when OSHA came to do a stack test?

B. Hobby: Yes. Well they would do a stack test, but it actually wouldn’t be a stack test, because most of the time they would do the stack test, the pond water would be cut off, and it would be only fresh water going into the stack.

Attorney: Would Occidental know in advance, to your knowledge, when OSHA would come — Would they have advance notice?

B. Hobby: Yes. They’d have –

Attorney: What is the significance of shutting down the pond water and using fresh water instead for a stack test?

B. Hobby: Well, I know that fresh water is good and drinkable, pond water has got acid in it, and you can’t drink it, it burns if you get it on you. They use it to clean out tanks, railroad cars, and scrubbers because of the acid in it — it works good as a cleaner.

(Evaporation pond water is laden with phosphoric acid, and numerous

contaminants, including high concentrations of fluorine. Using pond water in the pollution scrubbers is like attempting to wash clothes in dirty water because the water has close to the limit of dissolved solids that it can hold.)

Attorney: What’s in the pond water to your knowledge?

B. Hobby: Acid.

Attorney: How did the acid get in the ponds?

B. Hobby: It goes through the scrubbers.

Attorney: The pond water would go through the scrubbers?

B. Hobby: Yeah.

Attorney: When OSHA wasn’t coming — did the plant use pond water?

B. Hobby: They normally used pond water.

Attorney: Did OSHA test, to your knowledge, the tanks when they would come to do — investigations?

B. Hobby: Well with the stack tests, they usually tested the whole plant, all the areas, some tanks. All the areas are tied into the stacks, but some tanks are blanked off. All of the fumes were blocked from going through the scrubber, and they just tested the stacks from the scrubbers, mostly.

Attorney: Do you have knowledge that anyone from Occidental volunteered to OSHA that the lines were shut down?

B. Hobby: No.

Attorney: Who shut the lines off? Did you ever shut the lines off?

B. Hobby: Yes. My crew. I blanked the lines sometimes.

Attorney: Who told you to shut the lines off?

B. Hobby: My supervisor. We’d be told that — at that time, those tanks needed to be blanked off, but common sense would tell you that they were talking about a stack test.

Attorney: Did you ever have to shut down the lines when OSHA wasn’t coming?

B. Hobby: When we had to go in and work on the tanks, but not when they were full. The only thing we would be doing when OSHA came in was blanking the lines. We would not be working on them.

Attorney: How many times did this happen, Mr. Hobby? Did you shut the lines down or instruct someone to do it?

B. Hobby: Every time they came in to do a stack test, however long — however often they would do the stack tests.

Attorney: You worked for Occidental for twenty plus years, what do you think would have happened to you, if you would have volunteered to OSHA that the lines were shut down of fresh water had been substituted for pond water?

B. Hobby: I wouldn’t be working there very long.

Attorney: Do you know anything else, or changes that occurred in the scrubbers before OSHA came for their inspections?

B. Hobby: Well, we’d have to pull out the main scrubber pads, and have them cleaned — cleaned real good, and make sure all of the pads were replaced, and fresh water was going to the scrubber.

Attorney: How often were the pads cleaned normally?

B. Hobby: When the exhaust fan would quit working.

Attorney: What would happen right before OSHA was coming for an inspection?

B. Hobby: They would be cleaned and the filter pads would be in place.

Attorney: Were they always in when OSHA wasn’t coming?

B. Hobby: No — like at the phosphoric acid plant, half the time, the pads would be pulled out because the fan couldn’t blow through them.

Attorney: How many times did you see OSHA come to Occidental where you or someone else at your instruction put fresh filter pads in, turn off the pond water and switch to fresh water, and/or shut down the lines? More than five? More than ten? More than fifteen?

B. Hobby: I would be guessing if I went any higher.

 … … …

The following segment concludes his deposition by his attorney.

The cross examination is redundant and offers no substantive insights.

Pages 141-143

Attorney: Are you through with your chemo at Shands?

B. Hobby: No. I go in the day after tomorrow for five days.

Attorney: Is your health insurance paying for it?

B. Hobby: Right now they are.

Attorney: What do you mean, right now, have you been told the insurance was going to be cut off?

B. Hobby: Well, I’ve been out of work for two years, it will automatically be cut off.

Attorney: What physical problems are you having now?

B. Hobby: My back, my side, my head, my feet.

Attorney: Feeling tired?

B. Hobby: All the time. I can’t do anything with my kids like I used to.

Attorney: How are you doing emotionally?

B. Hobby: I’m not.

Attorney: I think I know what you mean, but can you explain it for us on the record?

B. Hobby: I’m trying to hold up because of my kids, but it’s hard, because I can’t do anything with them like I used to.

Attorney: At that point in time, did you know unequivocally that working at Occidental and being exposed to this or that chemical caused what you currently have?

B. Hobby: When I was working out there, no, I thought it was the greatest place in the world to work.

Bobby Hobby worked in the maintenance department at Occidental for twenty-three years. The first eight years he had worked there; he did not know what a respirator was. Hobby and his coworkers were sent into tanks to weld with little or no ventilation and many were filled with fumes from phosphoric acid production. The dusts, fumes and vapors contained high levels of fluorine, radionuclides and sulfur dioxide. OSHA inspections were basically a joke in light of the fact that they have to give advanced notice of an inspection. Florida Department of Environmental Regulation does little or nothing to enforce any regulations regarding the phosphate fertilizer industry, and allows the industry to be self policing.

For Bobby Hobby and his coworkers, it is like the state and federal governments conspired against them. The U.S. Centers for Disease Control was aware of the high incidence of cancers among the population surrounding the Occidental Complexes, but the government-funded study suggested that poverty was the cause of the cancers. It also seems like the doctors and hospitals conspired against them. They were aware of the high rates of chronic illnesses among the workers, but it was almost always attributed to everything else except exposure to chemicals.

No one knows how many people have died or how many people are ill in Hamilton and the surrounding North Florida Counties because of Occidental’s wholesale pollution and chemical poisoning of the workers in order to turn a profit.

Not many people care, because they think: “It’s not in my back yard.” However, thousands of gallons of the very same pollution is being dumped into water supplies in the U.S. and Canada daily. It may take a little longer to catch up with the unconcerned, and the doctors will not have a clue as to what the cause of that odd malady is. The consequences of consuming the pollution, may have already affected you or someone close to you. No one knows the consequences of using the pollution as a fluoridation agent, because there has not been one clinical study with the toxic waste.

For the phosphate fertilizer industry, water fluoridation is an efficient, cost-effective solution for dumping pollution because for every pound of the fluoride ion, the industry also gets rid of another 5.8 pounds of pollution in the drinking water. The USEPA and U.S. Centers for Disease Control and Prevention say that there is nothing in the fluoridation agent that will hurt anyone: the very same statement that Occidental Chemical Corporation told the employees about the same pollutants. The American Dental Association unequivocally states that adding the pollution to drinking is the most significant preventive public health measure of our time.

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❝ If this stuff  [Fluoride] gets out into the air, it’s a pollutant;

If it gets into the river, it’s a pollutant;

If it gets into the lake, it’s a pollutant;

But if it goes right straight into your drinking water system,

it’s not a pollutant. That’s amazing! ❞

Dr. Hirzy 2000 Senior Vice-President of  EPA Headquarters Union.

CORRODED-STRIP

FLUORIDATION AND POLONIUM-210

 See more info on phosphate fertiliser

 ↓ ↓ ↓

   http://www.fluoridealert.org/phosphate/overview.htm

See also → Fluoride Emissions From Mt. Etna

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