Water Treatment With Silicofluorides And Lead Toxicity
Authors: Roger D. Masters and Myron J. Coplan
(Roger D. Masters – Research Professor -Nelson A. Rockefeller Professor of Government, Emeritus Dartmouth College)
Abstract:
Toxic metals like lead, manganese, copper and cadmium damage neurons
and deregulateneurotransmitters like serotonin and dopamine
which are essential to normal impulse control and learning.
Earlier studies show that — controlling for socio-economic and demographic factors — environmental pollution with lead is a highly significant risk factor in predicting higher rates of crime, attention deficit disorder or hyperactivity, and learning disabilities. Exposure and uptake of lead has been associated with industrial pollution, leaded paint and plumbing systems in old housing, lead residues in soil, dietary habits (such as shortages of calcium and iron), and demographic factors (such as poverty, stress, and minority ethnicity). We report here on an additional “risk co-factor” making lead and other toxic metals in the environment more dangerous to local residents: the use of silicofluorides as agents in water treatment. The two chemicals in question — fluosilicic acid and sodium silicofluoride — are toxins that, despite claims to the contrary, do not dissociate completely and change water chemistry when used under normal water treatment practices. As a result, water treatment with siliconfluorides apparently functions to increase the cellular uptake of lead. Data from lead screening of over 280,000 children in Massachusetts indicates that silicofluoride usage is associated with significant increases in average lead in children’s blood as well as percentage of children with blood lead in excess of 10μg/dL. Consistent with the hypothesized role of silicofluorides as enhancing uptake of lead whatever the source of exposure, children are especially at risk for higher blood lead in those communities with more old housing or lead in excess of 15 ppb in first draw water samples where silicofluorides are also in use. Preliminary findings from county-level data in Georgia confirm that silicofluoride usage is associated with higher levels of lead in children’s blood. In both Massachusetts and Georgia, moreover, behaviors associated with lead nurotoxicity are more frequent in communities using silicofluorides than in comparable localities that do not use these chemicals. Because there has been insufficient animal or human testing of silicofluoride treated water, further study of the effect of silicofluorides is needed to clarify the extent to which these chemicals are risk co-factors for lead uptake and the hazardous effects it produces.
Keywords: Lead; toxicity; pollution; children’s health; public water supplies
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” FLUORIDES, THE DEADLY TOXIN WITHIN ”
By Professor Dzulkifli Abdul Razak
National Poison Centre
Universitiy Sains Malaysia -
2 September 2001
The ability of fluoride to reduce thyroid hormone levels
has been know for over 100 years (Maumene 1855) —
Following the recent withdrawal of the cholesterol-lowering drug Lipobay, there is now a new perspective to the issue, the drug being a fluoride-containing compound. The drug, also known by its generic name, cerivastatin, is one of the many such compounds pulled off the shelves in the last few years.
Cerivastatin was taken off because of at least 40 deaths worldwide, 31 in the US alone. According to a recently released commentary by a Canadian group, Parents of Fluoride Poisoned Children, a series of fluoride containing drugs or so-called fluorinated drugs have been withdrawn from the market in the last 10 years due to their toxic effects on human beings. One notable example is the combination “Fen-Phen” (a generic combination of fenfluramine and phentermine, the former being a fluorinated drug type) which was said to have weight-reducing effects. Others are dexfenfluramine (Redux) and fenfluramine (Pondimin).
There are at least eight other examples of fluorinated drugs withdrawn so far, because serious side effects on the heart, and for suspected adverse influence on thyroid hormone activity.
They include, last year, cisapride (Propulsid) because of its severe side-effects on the heart. In 1999, two drugs were withdrawn.
These were an anti-allergy drug, astemizole (Hismanal); and grepafloxacin (an antibiotic, Raxar) because they too were associated with similar adverse events.
In 1998, patients with congestive heart failure using the drug mibedrafil (Posicor) showed a trend to higher mortality, causing it to be withdrawn.
Alredase (Tolrestat, an anti-diabetic) was withdrawn in 1997 after the appearance of severe liver toxicity and deaths among several patients. In the same year too fenfluramine (part of Fen-Phen) and dexfenfluramine were withdrawn.
In 1993, flosequinan (Manoplax, a heart drug) was withdrawn when it was shown that the beneficial effects on the symptoms of heart failure did not last beyond the first three months of therapy. After that, patients had a higher rate of hospitalization than patients taking a placebo.
Of the many fluorinated drugs that remain in the market some carry warnings of serious cardiac toxicity, for instance halofantrine, a schizonticidal drug. More specifically, other fluorinated drugs, although they have not yet been withdrawn, are known to cause muscle wasting or rhabdomyolysis; like cerivastatin.
For instance, the PFPC commentary noted that the fluorinated antibiotic fluoroquinolone, used to treat infections, is reported to cause tendonitis and rhabdomyolysis. In fact product information for such antibiotics (enoxacin, fleroxacin, norfloxacin, sparfloxacin, and tosufloxacin) was amended in Japan in October 1994, to state that rhabdomyolysis may occur. Reportedly, the tragic story involving fluorinated drugs (the fluorophenyls in particular, initially limited to industrial use involving dyes and pesticides) can be traced way back to the 1930s when they were used to treat hyperthyroidism.
The use followed a discovery by IG Farben (Bayer) and Knoll’s scientists that all fluoride compounds can interfere with thyroid hormone activity.
In the liver especially, organic fluoride compounds undergo extensive transformation, mainly via oxidative demethylation, involving the thyroid hormone (T3) mediated P-450 enzyme system. And the resulting metabolites may have higher activity and/or greater toxicity than the original compound.
The activity of organic fluoride compounds on the P-450 enzyme system is critical as it relates to the elimination of many other drugs. Inhibition of these enzymes can cause other drugs to accumulate to dangerous levels in the body, leading to hazardous drug interactions. In many cases fluorinated drugs are being implicated as documented in hundreds of well-established studies.
Moreover, adds PFPC, the metabolites produced by organic fluoride compounds in the liver can be transferred to the fetus through various pathways, including circulatory via placental passage, gastrointestinal via fetal swallowing, and respiratory secondary to fetal lung absorption. This may lead to congenital abnormalities as in the case of fluconsazole (Diflucan).
In short, going by the above evidence, fluorinated drugs seem to pose a number of risks associated with the fluorine or fluoride contained in them. It raises even more concern when fluoride itself is present in many industries and products, including food and drinks, without any rigorous evaluation or monitoring.
Of late, we have managed to label all toothpastes containing fluoride in this country. But this is clearly a minuscule effort in the attempt to regulate the use of fluoride as an inherent poison. We need to do more now.
For more information, contact the National Poison Centre at Universiti Sains Malaysia,
tel: 04-657 0099, fax: 04-656 8417,
Source: New Sunday Times (Focus) 2 September 2001
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