On 7 Mar 2003 13:36:47 -0800, gmp@adres.nl (Hua Kul) wrote:
>Alf Christophersen <alf.christophersen@basalmed.uio.no> wrote
>in message
>news:<kbnc6vsnnvq1mgb0op73j1cpdh415jkbf2@4ax.com>...
>> On Wed, 5 Mar 2003 13:33:31 -0600, "Scott T. Jensen"
>> <stj@charter.net> wrote:
>>
>> >Been hearing about the risks of aluminum, namely how it
>> >might be linked to Alzheimer's Disease. All my pans, pots,
>> >and silverware are made out of aluminum. Do I have
>> >anything to be concerned about? Will this be viewed by our
>> >descendents like how lead jugs, cups, water pipe systems,
>> >etc. of ancient Rome is viewed by us today?
>>
>> If dangerous, only antacid preparats would be of any
>> danger. These are pure aluminium salt preparates. Pans etc.
>> has a layer of alimunium oxide outmost and this is very
>> tough against chemical attacks, but pure, metallic Hg may
>> displace the layer and expose pure Al against water, which
>> make a noisy reaction possible :-) (nonoxidized Al is very
>> reactive towards water and form Al(OH)3 easily, if it
>> wasn't that it within nanoseconds reacts with O2 to form
>> the oxide instead. Also extreme heating of pan can expose
>> pure Al if you heat a pan until glowing and then pour water
>> in it, the water (in addition to the instant vaporisation
>> due to the heat) will react fiercely with the Al to form
>> Al(OH)3
>>
>> Al theory as reason for Alzheimer has been disproven by
>> the way.
>
>
>Hello Alf. I usually agree with your posts, but I can't
>accept your last statement. I don't believe Al has been ruled
>out as a cause of Alzheimer's, although it hasn't been proven
>yet. Another way that Al appears to be dangerous is the
>production of aluminum fluoride when fluoridated tap water is
>boiled in aluminum pans. In one study, the reference to which
>I can't locate at the moment, "boiling fluoridated tap water
>in an aluminum pan leached almost 200 parts per million (ppm)
>of aluminum into the water in 10 minutes. Leaching of up to
>600 PPM occurred with prolonged boiling. Different releases
>of aluminum depend upon the composition of the pan and the
>type of food being cooked. Using non-fluoridated water showed
>almost no leaching from aluminum pans."
>(http://www.mercola.com/2001/may/16/fluoride.htm) As far as
>I'm concerned, there is enough evidence for harm that I avoid
>fluoridated water and aluminum cookware. But that's just me.
So you avoid "chloridated" water too?
If boiling in one ppm sodium fluoride dissolves some
aluminium, then surely several hundred ppm sodium chloride is
going to dissolve more. I think that food acids will be so
much more potent at this dissolution. Aluminium is virtually
unavoidable in the environment. Just because it appears in
certain diseased states seems to me to be extremely remote
causatively.
>"Epidemiologic data suggest that Al exposure via drinking
>water is associated with an increased incidence of AD
>(McLachlan, 1995).
What about aluminium in food? What about kaolin given for the
trots? Antacids?
>The data are problematic with respect to duration of exposure
>and show an association rather than causality, although some
>indication of a dose trend was seen in five of eight studies
>as noted above (Nieboer et al., 1995)(Table 5). On the basis
>of the experimental database, McLachlan (1995) has
>recommended a lowering aluminum exposure in municipal
>drinking water to below 50 mg/L, at least in the province of
>Ontario, Canada.
Some public health measures are extreme, for public
perception, not scientific reasons.
BTW, 50 mg/l (ppm) is 50 times the normal fluoridation
concentration.
>Alternatively, Nieboer et al. (1995) support strict
>enforcement of a 100 mg/L drinking water guideline.
That's over three ounces of aluminium in a unit of water
purchased (1000litres) (NaF is added at one thirtieth of an
ounce to this same amount of water) I wouldn't think it
matters much. How on earth do you get that much aluminium in
solution? Most of our water supplies are stored in
aluminosilicate storage tanks (earth dams)
>The devastating nature of the disease, the lack of an
>effective treatment or prevention, and the high cost to the
>health care system were cited as factors weighing against the
>moderate cost of reducing aluminum in drinking water
>(McLachlan, 1995).
Lime the water -- increase the pH. But only to calm the folks
who think the sky is falling.
>Another observation linking Al neurotoxicity to AD is that of
>a clinical trial involving the treatment of AD with the Al
>chelator desferrioxamine (McLachlan et al., 1991; Savory et
>al., 1998). While the beneficial effects noted on AD could
>have been due to reducing oxidative stress-induced neuronal
>damage, it seems more likely to have been related to Al
>removal. As noted above there is no substantiated mechanism
>for AD, however the possible role of Al as one of several
>factors in the tau-AD disease link should not be ignored
>(Savory and Garruto, 1998). Although it has not been
>established that AD is a result of Al intoxication, there is
>considerable evidence that Al is neurotoxic in man.
Or just happens to appear when this damage is apparent? Look
at the actual damage and find what other elements are in
different concentrations. Circumstantial evidence. They may
just appear because of the disease state, and have nothing to
do with the cause. If Al was the cause, there would surely be
much more AD.
>Perl et al. (1982) showed prominent accumulation of Al within
>the nuclear region and perikaryal cytoplasm of
>neurofibrillary tangle-bearing neurons in patients with ALS
>and Parkinsonism-dementia of Guam. High levels of Al and
>unusually low levels of calcium and magnesium have been found
>in samples of drinking water and garden soils from Guam.
>Studies measuring trace elements in subcellular compartments
>demonstrated increased Al and Fe concentrations in Lewy
>bodies (Hirsch et al., 1991), which are a hallmark of
>Parkinson’s disease (PD), and in the neuromelanin
>granules of neurons in the substantia nigra of patients with
>PD (Good et al., 1992a,b). Thus, aluminum, in conjunction
>with different modes of action in each disease, may
>contribute to the cascade of events which eventually results
>in neuron death in AD, PD, and the Guam PD/ALS syndrome
>(McLachlan, 1995).
>
>Altmann et al. (1999) conducted a retrospective study of
>neurological effects in a population accidentally exposed to
>aluminum sulphate in the drinking water. In 1988 20 tons of
>aluminum sulfate were accidentally emptied into a treated
>water reservoir that served 20,000 residents of the Camelford
>area of Cornwall in the United Kingdom. Early health
>complaints included rashes and gastrointestinal disturbances
>within days and later musculoskeletal pains, malaise, and
>impaired concentration and memory. Two years later 400 people
>were suffering from symptoms attributed to the incident. The
>retrospective survey involved 55 exposed adults three years
>after the incident and 15 unexposed siblings of similar age.
>The study included an assessment of premorbid IQ with the
>national adult reading test, a computerized battery of
>psychomotor testing, and measurement of the difference in
>latencies between the flash and pattern visual evoked
>potentials. The mean IQ was above average,
>114.4, siblings, 116.3. The most sensitive of the psychomotor
> tests for organic brain disease was the symbol digit
> coding test which has a normal score of 100, with
> abnormal less than 85. Exposed subjects performed badly:
> 51.8 ± 16.6 (SE) vs. 87.5 ± 4.9 (SE) for the unexposed
> siblings (p = 0.03). The flash-pattern differences in the
> Al-exposed group were greater than in 42 unrelated
> control subjects of similar age (p = 0.0002). The authors
> concluded that the aluminum sulfate water contamination
> incident probably led to long term cerebral impairment in
> some of the exposed people in Camelford. Although no
> additional follow up studies have been conducted,
> anecdotally, some affected individuals still have
> symptoms 11 years later."
> http://www.oehha.ca.gov/water/phg/pdf/Alumin.pdf
>
>The daily ingestion of Al by humans is estimated to be 30 to
>50 mg (National Library of Medicine 2000). The increase in Al
>exposure of the general population becomes of increasing
>concern with studies that suggest possible association
>between exposure and neurological diseases (Harris, Berthon
>et al. 1996; van Landeghem, D'Haese et al. 1997; Altmann,
>Cunningham et al. 1999).
>
>Toxicity of Al in humans is known to occur in at least two
>specific situations. Dementia in dialysis patients is related
>to Al exposure (van Landeghem, D'Haese et al. 1997;
>Suarez-Fernandez, Soldado et al.
>1999). A second prominent Al toxicity found in dialysis
> patients is osteomalacia or metabolic bone disease
> (Kausz, Antonsen et al. 1999) (Klein 1998). Preterm
> infants with parenteral administration of nutritional
> solutions are also at risk for Al-induced neurotoxicity
> (Hawkins, Coffey et al. 1994; Driscoll, Cummings et al.
> 1997). Al inhalation, especially in workers, may be
> associated with increased incidence of asthma
> (Sorgdrager, de Looff et al. 1998; Vandenplas, Delwiche
> et al. 1998). Pre-term infants are also at risk for
> Al-induced metabolic bone disease (Klein 1995; Klein
> 1998).
>
>Two studies in rats report enhanced mortality in rats exposed
>to 0.5 ppm AlF3 complexes in the drinking water (Varner,
>Horvath et al. 1994; Varner, Jensen et al. 1998). Recently,
>evidence of increased absorption of Al has also been
>demonstrated with an inorganic Al-complex, AlF3 . Fluoride
>also enhances the neurotoxicity of Al (van der Voet, Schijns
>et al. 1999). The potential relevance of such Al- complexes
>derives from the observation that under slightly acidic
>source water conditions organic Al-complexes and Al-F
>complexes predominate, and these can persist to a significant
>degree through drinking water treatment. http://ntp-server.n-
>iehs.nih.gov/htdocs/Chem_Background/ExSumPdf/Aluminumalt.pdf
>
>--Hua Kul
And AlCl3?
Moosh:)