KILLING and INJURING But its all in a GOOD CAUSE

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KILLING and INJURING But its all in a GOOD CAUSE

Various snippets on aluminium sulphate and its lethal potential

Note that WITHOUT the Camelford poisoning incident our knowledge would be

largely limited to that of the immense suffering by dialysis cases only.

The harm from Camelford has been ignored so our knowledge from this is sparse

and disputed.

Pyschiatrists of international repute (Simon Wesseley and trainer of

Fombomme?) DENY aluminium harm and most lessons we could have learned from

Camelford

are now LOST (but not burnt or stolen).

The INCHEM document contrasts with the first document on safety which tells us

nothing except dont worry.

The INCHEM document may not have been read by vaccine makers as the toxicity for

babies (they certainly didn't read of mercury harm in vaccines for 30 years) by

injection and as shown to dialysis patients is a very real, powerful and

immensely dangerous toxin at levels that make the aluminium in our vaccines look

like a marvellous

candidate for administering the death penalty in place of sea salt injections as

at present.

Harm shown from 60 parts per billion and less from current knowledge.

But some vaccines for infants contain 625 000 parts per billion with this dose

repeated time after time after time to infants in the first two years. Potential

for harm without

any need for synergy is quite quite remarkable.

WHO recommend a max of 200 parts per billion in water already above levels of

harm shown by researchers at 60 parts per billion. Obviously they think drinking

the stuff

is less hazardous than injecting it and they may well be correct. Well they

can't get it wrong all the time.

Consider:

'Dialysis dementia' involves the accumulation of aluminium, mainly in

the brain, in patients on haemodialysis

So we know that injections of any aluminium will have the potential to enter the

brain of those with established blood brain barriers so what is the potential in

infants with

no blood brain barrier. Life just gets easier or should that be DEATH.

This from 60ppb or less for adults but babies take 625 000 ppb on the chin and

in their arms legs and mouths without blinking an eyelid but often crying and

crying and

crying until exhausted. Still its good to be « protected ». But who is

protected by sending baby to an early death (Harry ) or a life on the ASD

spectrum?

Note also the total abandonment of aluminium in perspirants not because its

toxic but because it doesnt work? Now how have these manufacturers in Big Pharma

been

so easily fooled for generations?

If they are this stupid lets hops they won't take to injecting toxic levels of

mercury and alumumium in babies before they are even born. OOOPS!

Of course they wouldnt then add phosphorus, fluoride or lemon juice to enhance

the toxicity WOULD THEY? OOOPS! OOOPS! and OOPS!

Of course we do have the protection of vaccine regulators and legal laws so

perhaps the unchangeable nature of chemical reactions is controlled by these

regulators

and laws, so we have nothing to worry about. I mean these experts have 100's of

peer reviewed papers, have written the last three volumes of vaccine science so

perhaps there expertise takes precedence over simple schoolboy chemistry.

And of course if all else fails we have the protection of the vaccine courts to

gets fair and due compensation as per Mrs Sally who got double life for

two lost boys

after vaccines and a corrupt autopsy that left her body to rot and ferment for

weeks so they could find enough alcohol to make a couple of bottles of whisky.

(grapes or

almost anything left for a few weeks produces alcohol at the rate of millions of

molecules per second). Or better Mrs Fletcher who started a vaccine group and

after

merely 18 years obtained compensation at about 40 per cent of prices 20 years

ago and not enough to pay for her time and effort. At an average workmans slary

for

this time she could have earned this amount many times over.

Protection by money to pay for harm is ZERO.

And protection by safe vaccines is less than ZERO.

Read any small print and count the dead bodies from vaccine trials which were

ok'd as safe for mass injections into anybody except them.

2ppb mercury toxic but 25 000ppb in vaccines just fine.

And in 2010

60ppb aluminium is toxic but 625 000 in vaccines for baby just great.

FEEL the protection of experts, vaccine makers and those regulators at CDC that

we rely on for safety.

OMG I feel ill.

Of course my maths needs checking and it may be that the 625 000 is the amount

before harm and the 600 is what they put in our childs vaccines but I wouldn-

bet on it.

But I would bet that there are many bloggers out there who will tell you that if

600 is toxic then 625 000 will be just fine for baby because us chemists aren'

really good

chemists andve lost credibility. I had to smile when one of these was an

acknowledged expert and knew mercury was just fine and couldnt hurt you. He was

so

confident of this his family get the full blast of mercury from an emitter 200

yards from his house with no adverse effects to him or his wife.

So one day perhaps I will agree that 625 000 is good when 600 is bad but I am

still waiting for that cheque to come through in the post. Or for some

epidemiologists in

comes every day. (dolly boy RIP)

http://www.inchem.org/documents/ukpids/ukpids/ukpid34.htm

Uses

Aluminium sulfate is used in water purification and as a mordant in dyeing

and printing textiles. In water purification, it causes impurities to coagulate

which are removed

as the particulate settles to the bottom of the container or more easily

filtered. This process is called coagulation or flocculation.

When dissolved in a large amount of neutral or slightly-alkaline water,

aluminium sulfate produces a gelatinous precipitate ofaluminium hydroxide,

Al(OH)3. In dyeing and

printing cloth, the gelatinous precipitate helps the dye adhere to the clothing

fibers by rendering the pigment insoluble.

Aluminium sulfate is sometimes used to reduce the pH of garden soil, as

it hydrolyzes to form the aluminium hydroxideprecipitate and a

dilute sulfuric acid solution. An

example of what changing the pH level of soil can do to plants is visible when

looking at the Hydrangea macrophylla. The gardener can add aluminium sulfate to

the soil to

reduce the pH level which in turn will result in the flowers of the Hydrangea

turning a different color.

Aluminium sulfate is the active ingredient of some antiperspirants; however,

beginning in 2005 the US Food and Drug Administration no longer recognized it

as a wetness

reducer.

Aluminium sulfate is usually found in baking powder, where there is controversy

over its use due to concern regarding the safety of adding aluminium to the

diet.

In construction industry it is used as waterproofing agent and accelerator

in concrete. Another use is a foaming agent in fire fighting foam.

It is also used in styptic pencils, and pain relief from stings and bites.

It can also be very effective as a molluscicide, killing spanish slugs.

Symptoms

 irritation skin, respiratory system; skin burns

Target Organs

 Skin, respiratory system

Aluminium sulphate is relatively non toxic. In 1988, contamination of

drinking water with aluminium sulphate led to a variety of acute

symptoms (Lowermoor Incident Health Advisory Group, 1991)

MECHANISM OF TOXICITY

There is experimental evidence that aluminium inhibits bone

mineralization partly by the deposition of aluminium at the

osteoid/calcified-bone boundary thereby directly inhibiting calcium

influx, and partly by aluminium accumulation in the parathyroid glands

with suppression of parathyroid hormone secretion (Visser and Van de

Vyver, 1985; Berland et al, 1988; Firling et al, 1994).

Proposed mechanisms of aluminium-induced neurotoxicity include

free-radical damage via enhanced lipid peroxidation, impaired glucose

metabolism, effects on signal transduction and protein modification

and alterations in the axunal transport and phosphorylation state of

neurofilaments (Birchall and Chappell, 1988; Exley and Birchall, 1992;

Erasmus et al, 1993; Winship 1993; Haug et al, 1994; Joshi et al,

1994; Strong, 1994).

TOXICOKINETICS

Absorption

In a healthy adult only approximately 15 µg of the average daily

dietary aluminium intake of 3-5 mg is absorbed (Winship, 1992). The

intestinal absorption of aluminium is enhanced by citrate which is

found frequently in effervescent drug formulations.

Main and Ward (1992) reported a reversible increase in the serum

aluminium concentration from 67.5 to 499.5 µg/L in a patient on

haemodialysis taking oral aluminium hydroxide when she was also given

an effervescent analgesic containing sodium citrate. Conversely the

bioavailability of aluminium in aqueous solution is greatly reduced by

silica, such that the toxicity of aluminium-containing phosphate

binders may be reduced significantly by the co-administration of

dissolved silica (Birchall, 1993).

In dialysis patients with aluminium overload, endogenous silicon may

serve a protective role in limiting tissue aluminium uptake (Fahal et

al, 1994). There may also be implications for domestic water supplies

if a high silicic acid concentration evades any hazards posed by

aluminium sulphate in water (Birchall, 1993).

Distribution

More than 90 per cent of absorbed aluminium is bound to transferrin

which does not cross the blood-brain barrier readily. The remaining

ten per cent is associated with low molecular weight complexes, such

as citrate, which can accumulate in brain tissue. In the body

aluminium is stored mainly in bone and liver.

Excretion

Aluminium is excreted predominantly via the kidneys and therefore will

accumulate in patients with renal failure (Alfrey, 1980). Preterm

infants also have a limited ability to excrete aluminium and there are

reports of accumulation in infants on long-term parenteral nutrition

(Sedman et al, 1985). Tsou et al (1991) demonstrated significantly

higher plasma aluminium concentrations (mean 37.2 µg/L) in normal

infants receiving oral aluminium-containing antacids for a prolonged

period compared to controls but this was not associated with adverse

clinical effects.

Ingestion

Acute aluminium sulphate ingestion causes primarily gastrointestinal

upset though neuropsychological and musculoskeletal sequelae were also

reported in those who drank water to which 20 tonnes of eight per cent

aluminium sulphate had accidentally been added in Camelford, Cornwall

in 1988 (see below). However, a group reviewing this incident

concluded that although " early symptoms, such as gastrointestinal

disturbances, rashes and mouth ulcers, could probably be attributed to

the toxic effects of the incident....The research reported to us does

not provide convincing evidence that harmful accumulation of aluminium

has occurred, nor that there is greater prevalence of ill-health due

to toxic effects of the water in the exposed population " (Lowermoor

Incident Health Advisory Group, 1991).

Gastrointestinal toxicity

Following the Camelford incident a variety of acute symptoms were

reported (Eastwood et al, 1990; Lowermoor Incident Health Advisory

Group, 1991), mainly mild gastrointestinal disturbance and mouth

ulcers (McMillan et al, 1993b). Water aluminium concentrations

recorded at the time ranged from 30 to 620 mg/L (WHO recommended

maximum aluminium concentration in drinking water is 200 µg/L)

(Eastwood et al, 1990; WHO, 1993). The low pH of the water also led to

leaching of other metals, such as copper, from the distribution pipes

so that those washing in the water developed green-discoloration of

their hair.

Substantial ingestion of aluminium sulphate causes burning in the

mouth and throat, gingival necrosis, nausea, vomiting, diarrhoea,

abdominal pain and, in severe cases, haemorrhagic gastritis with

circulatory collapse (Gosselin et al, 1984; Royal Society of

Chemistry, 1989; Meditext, 1995).

Spira (1933) reported dry mouth and throat, anorexia, nausea and

vomiting, glossitis, stomatitis, gingivitis and hiccup (in addition to

cutaneous and neurological symptoms) suspected to be caused by the

ingestion of elemental aluminium plus " aluminized " tap water. There

are, however, no case reports of substantial aluminium sulphate

ingestion in the literature over at least the last 30 years.

Neuropsychological toxicity

McMillan et al (1993b) reported " possible impairment of memory " in

those who drank aluminium sulphate-contaminated water in Camelford.

Serial neuropsychological assessments of 10 individuals between eight

and 26 months after the incident showed mild cognitive impairment but

a causal link with aluminium exposure could not be verified and in no

patient was there evidence of residual aluminium in bone or plasma

McMillan et al, 1993b).

Retrospective psychological testing on 39 children from schools in the

contaminated area showed no significant differences compared to

unexposed children (McMillan et al, 1993a). Muscle twitching, limb

paraesthesiae, arthralgia, neuralgia, giddiness, depression and

lassitude have been attributed to the ingestion of elemental aluminium

and aluminium contaminated tap water (Spira, 1933) but this was

speculative.

Musculoskeletal toxicity

Some individuals who drank the aluminium sulphate-contaminated water

in Camelford later complained of joint and muscle pains and fatigue

(Anonymous, 1991; McMillan et al, 1993b).

Bone toxicity

Bone biopsies some six months after the Camelford incident from two

individuals who drank the contaminated water showed increased

aluminium staining in bone formed at a time compatible with exposure

but normal bone aluminium concentrations overall, suggesting increased

aluminium absorption and retention following acute ingestion without

apparent adverse sequelae (Eastwood et al, 1990).

Neuropsychological toxicity

Aluminium sulphate is widely used in water purification. This source

has in the past contributed to aluminium toxicity in haemodialysis

patients (see below) and may be involved in the pathogenesis of

Alzheimer's disease via accumulation of aluminium in the brain but

this remains a highly contentious issue (Ebrahim, 1989; Petit, 1989;

Murray et al, 1991; Crapper McLachlan, 1994; Munoz, 1994).

Martyn et al (1989) and Neri and Hewitt (1991) reported a geographical

relationship between Alzheimer's disease and the concentration of

aluminium in drinking water but Wood et al (1988) found no significant

difference in mental test score between hip fracture patients living

in high versus low water aluminium areas.

Animal studies have demonstrated the ability of aluminium to induce

the formation of neurofibrillary tangles (Klatzo et al, 1965), impair

the learning ability of rats, and increase brain acetylcholinesterase

activity in a similar way to that seen in Alzheimer's disease

(Bilkei-Gorzó, 1993).

Other workers have shown elevated aluminium concentrations in brain

tissue from patients with Alzheimer's disease (Crapper et al, 1973)

and laser microprobe studies have demonstrated aluminium accumulation

in the neurofibrillary tangles of these patients (Good et al, 1992).

Harrington et al (1994) described Alzheimer's-disease-like

pathological changes in the brains of renal dialysis patients in

association with aluminium accumulation without clinical evidence of

dialysis encephalopathy (see below).

INJECTION

Neuropsychological toxicity

'Dialysis dementia' involves the accumulation of aluminium, mainly in

the brain, in patients on haemodialysis where the dialysis water

contains significant amounts of aluminium sulphate (McDermott et al,

1978). This should now be avoidable by reverse osmosis or deionization

of dialysis water prior to use.

Peritoneal dialysis solutions and haemofiltration and plasma exchange

substitution fluids also may contain excessive aluminium although the

incidence of toxicity from these preparations is small (Mion, 1985;

Mousson et al, 1989).

Elliott et al (1978a) reported a significant correlation between serum

aluminium concentrations and the concentrations of aluminium in the

water supply in eight patients on home dialysis with cases of dialysis

dementia confined to regions with high water aluminium concentrations

(>350 µg/L).

A larger study (Registration Committee of the European Dialysis and

Transplant Association, 1980) of patients treated in 65 dialysis

centres in Europe in 1976 and 1977 identified 150 cases of dialysis

dementia with a clear association between the occurrence of dementia

and dialysis with water which was not treated by deionization or

reverse osmosis. Only 23 of 150 patients were still alive in 1978.

Similar findings were reported by on et al (1982).

Although the problem of aluminium contamination of dialysates has

reduced in recent years, these patients may still accumulate aluminium

via oral aluminium hydroxide given as a phosphate binder (Salusky et

al, 1991). The contribution this makes to dialysis dementia is likely

to be small (McDermott et al, 1978; Registration Committee of the

European Dialysis and Transplant Association, 1980).

It has been suggested (Hodge et al, 1981) that to ensure no aluminium

uptake by dialysis patients, the dialysate aluminium concentration

should not exceed 14 µg/L. This corresponds to a maximum aluminium

concentration in the water supply of 5 µg/L since aluminium is present

in significant quantity in the dialysate concentrate (Hodge et al,

1981). The WHO recommended maximum aluminium concentration in drinking

water is 200 µg/L (WHO, 1993).

Dialysis dementia is progressive and often fatal (Alfrey et al, 1976;

Burks et al, 1976). In a review of 412 dialysis patients admitted to

one renal unit since 1972, Garret et al (1988) described 38 cases. The

mean time between onset of regular dialysis and development of

symptoms was 40 months with speech difficulties, seizures and

myoclonus the most common presenting features. Dyspraxia, involuntary

movements, poor concentration, loss of short-term memory, confusion,

depression and anxiety were also described and only nine patients were

still alive at the conclusion of the study (Garret et al, 1988).

The neurological consequences of aluminium intoxication may be

exacerbated in patients with aluminium bone disease who sustain

fractures, probably via increased bone aluminium mobilization

(Davenport and Ahmad, 1988).

There are reports of impaired cerebral function in haemodialysis

patients who have an increased body burden of aluminium but no

evidence of " dialysis dementia " (Altmann et al, 1989; Bolla et al,

1992). Altmann et al (1989) found significant abnormalities of

psychomotor function in 27 long-term haemodialysis patients who had

only mildly raised serum aluminium concentrations (mean 59 ± (SEM) 9

µg/L, normal < 10 µg/L).

In another study, 23 haemodialysis patients accidentally exposed to

aluminium for up to six months following failure of a reverse osmosis

system had a mean serum aluminium concentration of 147.3 ± (SEM) 11.7

µg/L without apparent neuropsychiatric sequelae (Caramelo et al,

1995).

Bone toxicity

In patients with renal failure aluminium toxicity may contribute to

renal osteodystrophy (Goyer et al, 1994). In a survey conducted by the

European Dialysis and Transplant Association, 102 of 150 patients with

dialysis dementia also had evidence of bone disease (Registration

Committee of the European Dialysis and Transplant Association, 1980).

Parkinson et al (1979) demonstrated a significant correlation

(p = 0.01) between the mean aluminium content of the water supply and

the incidence of fracturing dialysis osteodystrophy in 1293 patients

undergoing intermittent haemodialysis and Ward et al (1978) reported

significantly fewer cases of osteomalacia in patients maintained on

regular haemodialysis in Newcastle when the dialysate water was

deionised. Another study (Chan et al, 1990) found that the incidence

of osteomalacic fractures in dialysis patients could not be explained

by the aluminium concentration in dialysate alone and a significant

contribution by oral aluminium hydroxide was suggested.

Aluminium associated osteomalacic osteodystrophy is progressive and

characterized by bone pain, a proximal myopathy and spontaneous

fractures. In a review of skeletal surveys of 67 patients with

end-stage renal failure Garrett et al (1986) found that moderate or

severe fracturing osteodystrophy with greater than five fractures had

a diagnostic specificity for aluminium intoxication of 100 per cent,

provided trauma could be excluded.

Investigations typically show normal or only slightly increased

alkaline phosphatase activity, normal serum calcium and normal or

slightly high serum phosphate concentrations with reduced circulating

parathyroid hormone and increased bone and serum aluminium

concentrations (Winship, 1992). It is resistant to treatment with

vitamin D but improvement may follow desferrioxamine therapy as

discussed below.

Cardiovascular toxicity

Elliott et al (1978b) proposed aluminium induced cardiotoxity (via

inhibition of magnesium and ATP-dependent enzymes) as a contributing

factor in the sudden death of five dialysis patients, four with

dialysis encephalopathy and one non-encephalopathic patient whose

serum aluminium concentration was 600 µg/L.

Haemotoxicity

Aluminium intoxication may exacerbate the microcytic hypochromic

anaemia of chronic renal failure via impaired iron utilization

(Caramelo et al, 1995). This effect is at least partly reversible with

desferrioxamine therapy as discussed below.

Dermal toxicity

Brown et al (1992) suggested aluminium overload as the cause of a

widespread pruritic nodular rash (prurigo nodularis) in three patients

on maintenance haemodialysis. The serum aluminium concentration,

measured in two patients, was normal but complete resolution occurred

in all cases following weekly treatment for some three months with one

gram intravenous desferrioxamine.

Injection

Most cases of aluminium intoxication following aluminium sulphate

exposure occur in renal dialysis patients exposed to either

intravenous or intraperitoneal aluminium-containing dialysates. The

oral administration of aluminium containing phosphate binders may

exacerbate aluminium accumulation in these circumstances.

Antidotes

There is some evidence that parenteral desferrioxamine therapy slows

the rate of cognitive deterioration in patients with Alzheimer's

disease (Crapper McLachlan et al, 1991; Crapper McLachlan et al, 1993)

but further studies are required.

Desferrioxamine and dialysis encephalopathy

McCarthy et al (1990) treated 28 dialysis patients suffering from

aluminium toxicity with long-term (mean 11.0 months) intravenous

desferrioxamine, initially at a mean dose of 41.7 mg/kg body weight

once weekly, increasing to a maximum dose of 60 mg/kg as tolerated.

After five to seven months of treatment serum aluminium concentrations

decreased from a mean of 401 µg/L to 245 µg/L. Four patients, who had

advanced dementia before treatment, died during the study period. With

desferrioxamine treatment seven of 28 patients showed neurological

improvement and 25 patients showed improved or stable muscle strength

and overall functional capacity. The authors concluded that whilst

long-term desferrioxamine therapy can be important in the treatment of

patients with significant aluminium exposure it should be employed

only when symptoms demand treatment and when patients can be monitored

regularly for desferrioxamine toxicity (McCarthy et al, 1990).

In 71 dialysis patients D'Haese et al (1990) demonstrated that a serum

aluminium concentration of 60 µg/L or greater identified

aluminium-related bone disease with 82 per cent sensitivity and 86 per

cent specificity. However, Gilli et al (1983) suggested serum

aluminium concentrations were unlikely to reflect total aluminium

accumulation in uraemic patients and Seyfert et al (1987) suggested

plasma aluminium concentrations were not reliable in the diagnosis of

aluminium-related bone disease. This author emphasised the importance

of bone biopsy as the definitive investigation for aluminium

osteomalacia and advocated the 'desferrioxamine test' as a useful

diagnostic tool.

KILLING and INJURING But its all in a GOOD CAUSE