Effects of Silico-fluorides

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http://books.nap.edu/openbook.php?record_id=11571 & page=209Fluoride in Drinking Water: A Scientific Review of EPA's Standards (2006) Board on Environmental Studies and Toxicology (BEST)Neurotoxicity and Neurobehavioral Effects (205-223)Effects of SilicofluoridesIt has been suggested that the silicofluorides used to fluoridate drinking water behave differently in water than other fluoride salts (see Chapter 2 for further discussion) and produce different biological effects. For example, adding sodium silicofluoride (Na2SiF6) or fluorosilicic acid (H2SiF6) to drinking water has been reported to increase the accumulation of the neurotoxicant lead in the body (Masters and Coplan 1999; Masters et al. 2000). This association was first attributed to increased uptake of lead (from whatever source) caused by fluoride. However, enhanced lead concentrations were found only when the water treatments were made with a fluorosilicate and in children already in a high-lead exposure group.Urbansky and Schock (undated, 2000) took exception to almost all aspects of the studies by Masters and Coplan on the fluorosilicates. They argued that, under the conditions prevailing at the time of the addition of silicofluorides to drinking water, silicofluorides would be completely hydrolyzed before they reached the consumer’s tap (Urbansky and Schock 2000). Measurement techniques and statistical methods were also questioned. Theyconcluded that there is no “credible evidence” that water fluoridation has any quantifiable effect on the solubility, bioavailability, or bioaccumulation of any form of lead.Another issue that has been raised about differential effects of silicofluorides comes from the dissertation of Westendorf (1975). In that study, silicofluorides were found to have greater power to inhibit the synthesis of cholinesterases, including acetylcholinesterase, than sodium fluoride (NaF). For example, under physiological conditions, one molar equivalent of silicofluoride is more potent in inhibiting acetylcholinesterase than six molar equivalents of NaF (Knappwost and Westendorf 1974). This could produce a situation in which acetylcholine (ACh) accumulates in the vicinity of ACh terminals and leads to excessive activation of cholinergic receptors in the central and peripheral nervous system. At high concentrations, agents with this capability are frequently used in insecticides and nerve gases. At intermediate concentrations, choking sensations and blurred vision are often encountered. Modifications of the effectiveness of the acetylcholinergic systems of the nervous system could account for the fact that, even though native intelligence per se may not be altered by chronic ingestion of water with fluoride ranging from 1.2 to 3 mg/L, reaction times and visuospatial abilities can be impaired. These changes would act to reduce the tested IQ scores. Such noncognitive impairments in children were reported in a meeting abstract (Calderon et al. 2000), but a full publication has not been issued. Extended reaction times have been associated with impaired function of the prefrontal lobes, a behavioral change not directly tied to alterations in IQ (Winterer and Goldman 2003). Because almost all IQ tests are “time-restricted,” slow reaction times would impair measured performance.An interesting set of calculations was made by Urbansky and Schock (undated)—namely, compilation of the binding strengths of various elements with fluorine. They studied eight different complexes. Aluminum and fluorine have the highest binding affinity. Fluorine also forms complexes with other elements including sodium, iron, calcium, magnesium, copper, and hydrogen. Associations with some of these other elements may have implications for some of the neurotoxic effects noted after fluoride or SiF exposure.DementiaFor more than 30 years it has been known that Alzheimer’s disease is associated with a substantial decline in cerebral metabolism (Sokoloff 1966). This original observation has been replicated many times since then. The decrease is reflected in the brain’s metabolic rate for glucose, cerebral rate for oxygen, and cerebral blood flow. In terms of reduced cerebral blood flow, the reduction found in Alzheimer’s patients is about three timesgreater than in patients with multi-infarct dementia. As early as 1983, Foster et al. (1983) demonstrated a general decline in the rate of utilization of glucose with the marker F-2-fluorodeoxyglucose with a positron-emission tomography scan. Recently, over and above the general decline in aerobic metabolism, several patterns of enhanced decreases in energy utilization have been demonstrated. The temporal, parietal, and frontal regions are areas with some of the greatest reductions (Weiner et al. 1993; Starkstein et al. 1995). It is possible that the decline in glucose utilization is an early sign of the onset of dementia (Johnson et al. 1988; Silverman and Small 2002). In addition there is evidence from a number of sources that alterations induced by Alzheimer’s disease can be observed in many body regions and in blood. This indicates that the disease has system-wide effects in the body. One system particularly sensitive to carbohydrate utilization is the collection of areas involved with the synthesis of ACh. The release of this transmitter is also negatively affected by the interruption of aerobic metabolism and the effect can be noticed in the projection fields of the cholinergic systems. Fluoride produces additional effects on the ACh systems of the brain by its interference with acetylcholinesterase.Most of the drugs used today to treat Alzheimer’s disease are agents that enhance the effects of the remaining ACh system. Nevertheless, it must be remembered that one certain characteristic of Alzheimer’s disease is a general reduction of aerobic metabolism in the brain. This results in a reduction in energy available for neuronal and muscular activity.Because of the great affinity between fluorine and aluminum, it is possible that the greatest impairments of structure and function come about through the actions of charged and uncharged AlF complexes (AlFx). In the late 1970s and through the early 1990s there was considerable interest in the possibility that elemental aluminum was a major contributing factor to the development of dementia of the Alzheimer’s variety as well as to other neurological disorders. In a study of more than 3,500 French men and women above the age of 65 (Jacqmin et al. 1994), a significant decrease in cognitive abilities was found when their drinking water contained calcium, aluminum, and fluorine. Only aluminum showed any relation to cognitive impairment and that depended on the pH of the drinking water being below 7.3. Curiously, at higher pH values, a favorable effect on cognitive actions was found. In recent work with animals, aluminum-induced behavioral changes similar to those found in human dementia, as well as correlated histological changes in animals’ brains, were found (Miu et al. 2003). Active research continues at the cellular level on the neural mechanisms disturbed by aluminum (Becaria et al. 2003; Millan-Plano et al. 2003). On the epidemiological side there are inconsistencies in the results of different studies. For example, a recent review concludes that “the toxic effects of aluminum cannot be ruled out either, and thus exposure to aluminum should be monitored and limited as far as possible” (Suay and Ballester 2002). In addition to a depletion of acetylcholinesterase, fluoride produces alterations in phospholipid metabolism and/or reductions in the biological energy available for normal brain functions (see section later in this chapter on neurochemical effects). In addition, the possibility exists that chronic exposure to AlFx can produce aluminum inclusions with blood vessels as well as in their intima and adventitia. The aluminum deposits inside the vessels and those attached to the intima could cause turbulence in the blood flow and reduced transfer of glucose and O2 to the intercellular fluids. Finally histopathological changes similar to those traditionally associated with Alzheimer’s disease in people have been seen in rats chronically exposed to AlF (Varner et al. 1998).http://books.nap.edu/openbook.php?record_id=11571 & page=209--~--~---------~--~----~------------~-------~--~----~To to this group, send email to: MedicalConspiracies- (AT) googl (DOT) com