Human Toxicity, Environmental Impact and Legal Implications of

HUMAN TOXICITY, ENVIRONMENTAL IMPACT AND LEGAL IMPLICATIONS OF WATER FLUORIDATION
networks adapt their short- and long-term responses to environmental stimuli,
represents a major component of neurological disease. 543
Activation of gene expression was shown to be involved in a large variety of
processes in both the developing and mature nervous system, including
proliferation of neuronal precursors, outgrowth of neuronal processes,
learning and memory in invertebrates and vertebrates, induction of
neurotrophic and neuroprotectant cellular programs and regulation of
circadian rhythms. 544 , 545 , 546 , 547 , 548
It is obvious that any scientifically documented substance that may
increase the associated risk of neurological disease, learning or memory
disabilities, sudden death syndrome (SDS) or other cardiovasculor
disease should in no circumstance be injected into the public drinking
water supplies.
This raises serious concerns for the possible health implications for high-risk
individuals in particular for infants who are bottle-fed formula milk
constituted with fluoridated water (exposing them to concentrations of
fluoride at multiples above the recommended tolerable daily intake)
and adults who consume large volumes of water (including active sport
enthusiasts) as well as diabetics with impaired renal kidney function (who
are already a high-risk sector for coronary disease).
These findings are of critical significance demanding, in the interests of
public health and safety, an immediate response from the Government
of Ireland requiring the immediate cessation of the water fluoridation
policy. In light of the information provided in this report failure to act by
the appropriate authorities may be deemed to be criminally and
professionally negligent.
543 Tardito D, Perez J, Tiraboschi E, Musazzi l, Racagni g, Popoli, M. Signalling Pathways
Regulating Gene Expression, Neuroplasticity, and Neurotrophic Mechanisms in the
Action of Antidepressants: Critical Overview, pharmacological Reviews Vol. 58, No. 1
544 Kandel ER (2001) The molecular biology of memory storage: a dialogue between
genes and synapses. Science (Wash DC) 294:1030–1038.
545 Mabuchi T, Kitagawa K, Kuwabara K, Takasawa K, Ohtsuki T, Xia Z, Storm D,
Yanagihara T, Hori M, and Matsumoto M (2001) Phosphorylation of cAMP response
element-binding protein in hippocampal neurons as a protective response after
exposure to glutamate in vitro and ischemia in vivo. J Neurosci 21:9204– 9213
546 Reppert SM and Weaver DR (2001) Molecular analysis of mammalian circadian
rhythms. Annu Rev Physiol 63:647–676.
547 Kida S, Josselyn SA, de Ortiz SP, Kogan JH, Chevere I, Masushige S, and Silva AJ
(2002) CREB required for the stability of new and reactivated fear memories. Nat
Neurosci 5:348–355
548 Pittinger C, Huang YY, Paletzki RF, Bourtchouladze R, Scanlin H, Vronskaya S, and
Kandel ER (2002) Reversible inhibition of CREB/ATF transcription factors in region CA1
of the dorsal hippocampus disrupts hippocampus-dependent spatial memory.
Neuron 34:447–462.
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