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Sunday, March 07, 2010

New fluoride-lead study cause for ending fluoridation

A very important new study has just been published, ahead of print, by the journal Toxicology, in February 2010:

Fluoride increases lead concentrations in whole blood and in calcified tissues from lead-exposed rats

By Sawana RMM (a), Leite GAS (a), Saraiva MCP (a), Barbosa Jr. F (b), Tanus-Santos JE (c), Gerlach RF (a)

(a) School of Dentistry of Ribeirao Preto, University of Sao Paulo
(b) School of Pharmaceutical Sciences of Ribeirao Preto, University of Sao Paulo
(c) Faculty of Medicine of Ribeirao Preto, University of Sao Paulo

The authors note that, "Higher blood lead levels have been reported in children living in communities that receive fluoride-treated water." They cite the two papers on Masters and Coplan (1999, 2000).

The authors designed an animal experiment to see whether fluoride co-administered with lead increases lead concentrations in blood and calcified tissues. It is important to note that the fluoride compound that they used was hexafluorosilicic acid, one of the silicon fluorides used as fluoridating agents in over 90% of the water supplies fluoridated in the US. Hitherto, nearly all animal experiments have used sodium fluoride.

METHOD: Four groups (i.e. a control group; a fluoride group; a lead group; a fluoride plus lead group) of female (Wistar) rats and their offspring were exposed to different drinking water preparations from 1 week prior to mating until offspring were 81 days old. The drinking water preparations used in the four groups were:
1) The Control Group received water containing maximally 0.1mg/L of fluoride and 0.5 µg/L of lead.

2) The Fluoride group (the F group) received water containing 100mg/L of fluoride (administered as hexafluorosilicic acid)

3) The Lead group (the Pb group) given 30mg/L of lead (administered as lead acetate)

4) The Combined Lead and Fluoride group (the F + Pb group) given 100mg/L of fluoride as hexafluorosilicic acid and 30mg/L of lead as lead acetate

Blood and calcified tissues (enamel, dentine, and bone) were harvested at day 81 for lead and fluoride analyses.

RESULTS: Higher blood lead concentrations (over three times) were found in the fluoride plus lead group compared with the lead group (76.7+/-11.0mug/dL versus 22.6+/-8.5mug/dL, respectively; p<0.001)." Two- to 3-fold higher lead concentrations were found in the calcified tissues in the fluoride plus lead group compared with the lead group (all p<0.001). Lead concentrations were found to be 2.5 times higher in the superficial enamel, 3 times higher in surface bone, 2 times higher in whole bone, and 1.7 times higher in the dentine when the animals were co-exposed to fluoride, thus indicating a consistent rise in the amounts of lead found in whole blood and calcified tissues in the F+Pb Group. CONCLUSIONS: The authors concluded: "These findings show that fluoride consistently increases blood lead and calcified tissues lead concentrations in animals exposed to low levels of lead and suggest that a biological effect not yet recognized may underlie the epidemiological association between increased blood lead levels in children living in water-fluoridated communities." Probably anticipating the usual criticism leveled against animal studies of this type by pro-fluoridation zealots, the authors of this study carefully address the issue of the concentrations of both lead and fluoride used in this experiment. They write:
The concentration of lead in drinking water used in the present study is considered a low concentration for rodents (Leasure et al., 2008). However, while the fluoride concentration used in the present study could be considered relatively high for rodents (100mg/L or ppm), this concentration was chosen because it produces plasma fluoride levels that are comparable with those commonly found in humans chronically exposed to 8mg/L of fluoride in the drinking water, which is a concentration known to cause severe fluorosis.

Since this study was based on a hypothesis derived from epidemiological evidence from thousands of children (that fluoride from the water might increase BPblevels), we felt that we had to maximize fluoride concentrations to observe its influence on lead levels in this proof-of-concept animal study. Although children are not chronically exposed to high concentrations of fluoride (100ppm) by means of drinking/cooking water, children are frequently exposed to high levels of fluoride during their first years because of the many sources of fluoride available to them. Since fluoride is not considered a toxic agent, it is widely available through mouth rinses, toothpastes, tablets, besides the fluoride present in drinking water, beverages, and food. Indeed, the widespread presence of fluoride increased the prevalence of fluorosis in the USA (Pendrys, 2000) and in other countries (Leverett, 1986; Jackson et al., 1999; Tabari et al.,2000; Tsutsui et al.,2000; Pereira et al.,2000). Therefore, it is likely that young children may experience episodes of exposure to high levels of fluoride, which may cause their BPb (blood lead) levels to increase and produce more lead toxicity.

A reason for major concern is the fact that exposure to increased amounts of lead and fluoride occurs at about the same age (1-3 years). Some studies of fluorosis prevalence point to a higher degree of fluorosis in front teeth and first molars (Ismail et al., 1990), which is an indirect measure of dose that indicates that the children receive the highest fluoride doses when their front teeth and first molars mineralize(at ages 1-5 years). This is about the same time when BPb levels are the highest in children. Infact, the exposure of children to lead apparently peaks at 12-36 months of age, which is the time when toddlers experience prominent hand-to-mouth behavior (Binns et al., 2007). Therefore, this is a critical time when systemic exposure to fluoride should be minimized, since fluoride may increase lead accumulation, and any preventable exposure to lead should be avoided (Binns et al., 2007).
FAN's comment: In essence these authors have provided a well-designed animal study supporting the epidemiological findings of Masters and Coplan.

No one can deny that even very low levels of lead exposure can compromise the intellectual development and behavior of young children. If, as this experiment shows in animals, and Masters and Coplan may have found in epidemiological studies, that lead exposure (from any source) is increased by the presence of fluoride in the water, in any rational world this should force the end of fluoridation immediately. What parent in their right mind would knowingly allow the possibility that their child's mental development be impaired in exchange for some slight and questionable benefit to their teeth. However, without the mainstream media and the majority of environmental organizations involved in this issue it is hard to get this information to parents. Thus the chances are that this study will be ignored, like the landmark NRC (2006) review, by those governments determined to continue fluoridation whatever the costs to public health.

As each new scientific study makes the practice of water fluoridation more and more unjustified one feels as if one is caught up in some Kafka novel. We are trapped by a text that was written in 1950 when the US Public Health Service endorsed fluoridation with practically no science on the table. This endorsement set off such a cascade of endorsement dominoes from "professional" bodies that no one seems to have the guts to say was a terrible mistake. All one's efforts to point out - like the little boy in Hans Christian Anderson's famous tale - that the emperor has no clothes are met by derision by the modern day courtiers at the CDC and the ADA. Science has been subordinated to authority and public policy has become the plaything of the arrogant.

Meanwhile, for those who care for their common man this study is another critically important piece of ammunition in the battle to end this sordid practice worldwide.

The abstract of the paper can be accessed at

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