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High aluminium content of infant milk formulas

Authors:

Abstract

The aluminium content of several commercially available infant milk formulas was measured by electrothermal atomic absorption spectrometry. Results were compared with those for fresh breast milk, cow's milk, and local tap water. Differences in aluminium concentration of greater than 150-fold were found, with the lowest concentrations in breast milk.
914
Archives
of
Disease
in
Childhood,
1986,
61
assessing
exercise
induced
bronchospasm
in
clinical
practice.
J
Allergy
Clin
Immunol
1979;69(6):609-11.
2
Godfrey
S.
Exercise
and
asthma.
In:
Clark
T,
Godfrey
S,
eds.
Asthma.
London:
Chapman
and
Hall,
1983:61.
Eggleston
PA,
Guerrant
JL.
A
standardised
method
of
evalu-
ating
exercise-induced
asthma.
J
Allergy
Clin
Immunol
1976;58:414-25.
4
Anderson
H,
Bailey
P,
Cooper
J,
Palmer
J,
West
S.
Medical
care
of
asthma
and
wheezing
illness
in
children:
a
community
survey.
J
Epidemiol
Community
Health
1983;37:180-6.
Wilson
BA,
Evans
TN.
Standardization
of
work
intensity
for
evaluation
of
exercise-induced
bronchoconstriction.
Eur
J
Applied
Physiol
1981;47:289-94.
6
Godfrey
S,
Silverman
M,
Anderson
S.
The
use
of
the
treadmill
for
assessing
EIA
and
the
effect
of
varying
the
severity
and
duration
of
exercise.
Pediatrics
1975;56(suppl):893-9.
Correspondence
to
Professor
R
D
G
Milner,
University
Depart-
ment
of
Paediatrics,
Children's
Hospital,
Sheffield
SlO
2TH,
England.
Received
24
May
1986
High
aluminium
content
of
infant
milk
formulas
R
WEINTRAUB,
G
HAMS,
M
MEERKIN,
AND
A
R
ROSENBERG
Departments
of
Nephrology
and
Clinical
Chemistry,
The
Prince
of Wales
Children's
Hospital,
Sydney,
New
South
Wales,
Australia
SUMMARY
The
aluminium
content
of
several
com-
mercially
available
infant
milk
formulas
was
measured
by
electrothermal
atomic
absorption
spec-
trometry.
Results
were
compared
with
those
for
fresh
breast
milk,
cow's
milk,
and
local
tap
water.
Differences
in
aluminium
concentration
of
greater
than
150-fold
were
found,
with
the
lowest
concen-
trations
in
breast
milk.
Because
of
its
ubiquitous
nature,
aluminium
has
not
traditionally
been
regarded
as
an
essential
trace
element.1
No
cases
of
aluminium
deficiency
have
been
reported
and
minimum
daily
requirements
for
different
ages
are
unknown.
Fluids
yielding
as
little
as
7*5-15
ig
of
aluminium
per
day
have
been
used
recently
without
detriment,
however,
in
infants
receiving
long
term
total
parenteral
nutrition.2
Aluminium
toxicity
in
patients
with
chronic
renal
insufficiency
undergoing
haemodialysis
or
ingesting
large
quantities
of
phosphate
binding
gels
is
well
recognised.3
Recently,
the
high
aluminium
content
of
a
proprietary
milk
formula
was
implicated
as
the
cause
of
aluminium
toxicity
in
two
infants
with
neonatal
uraemia.4
In
this
paper
we
report
the
results
of
the
measurement
of
aluminium
in
a
variety
of
infant
feeds.
Methods
Sample
collection
and
preparation.
Preprepared
liquid
and
powdered
formulas
were
sampled
either
directly
from
their
glass
containers
or,
in
the
case
of
preparations
in
cans,
by
collecting
aliquots
into
acid
washed
polystyrene
tubes.
Each
feed
was
sampled
on
two
occasions
and,
where
possible,
from
dif-
ferent
batches.
Breast
milk
was
collected
by
lactating
mothers
directly
into
acid
washed
polystyrene
tubes,
using
a
no
touch
technique.
The
powders
were
reconstituted
in
the
laboratory
by
adding
distilled,
double
deionised
(aluminium
free)
water,
using
acid
washed
volumetric
appar-
atus,
to
portions
of
accurately
weighed
milk
powder.
Aluminium
analysis.
Aluminium
was
assayed
by
graphite
furnace
atomic
absorption
spectrometry
employing
a
Varian
Techtron
AA975
and
GTA
95
with
autosampler.
All
samples
were
initially
diluted
in
the
ratio
of
1
volume
of
sample
to
14*2
volumes
of
0-3%
analytical
grade
hydrochloric
acid
on
an
automatic
diluter.
The
aluminium
content
of
samples
was
quanti-
tated
by
the
method
of
standard
additions
to
allow
for
the
variation
in
instrument
response
caused
by
the
different
sample
matrices.
Typically,
a
single
random
representative
sample
was
used
to
generate
a
standard
additions
calibration
curve
for
each
analytical
run.
Subsequent
samples
in
the
run
were
quantitated
by
comparison
with
this
curve.
Samples
yielding
a
mean
peak
height
absorbance
greater
than
the
highest
calibration
point
were
further
diluted
with
0-3%
hydrochloric
acid
until
they
fell
within
the
calibration
range.
The
analytical
technique
was
controlled
with
'in
house'
aqueous
and
serum
based
control
materials
(method
coefficient
of
variation
at
80
gg/l
was
roughly
10%,
run
to
run)
and
by
participation
in
a
national
aluminium
analysis
quality
control
survey
(Department
of
Applied
Biology,
Royal
Melbourne
Institute
of
Technology).
The
spectrometer
was
operated
in
peak
height
High
aluminium
content
of
infant
milk
formulas
915
Table
Comparative
aluminium
content
of
infant
feeds
Sample
Type
of
feedt
Aluminium
content
Country
of
origin
(tgllitre
of
feed)t
Powder
Liquid
(Itglg)
(ttglml)
Breast
milk
0.03
30
5%
glucose
0
04
35
Tap
water
(four
readings)
0 04
40
Glucose-electrolyte
mixture
0 04
40
'Locasol'
0-23 85
Holland
Pasteurised
cow's
milk
0-09
95
Australia
'De-Lact
Infant'*
0-50
105
Australia
'Lactogen'
0-17
105
Australia
'S26'*
0-14
125
United
States
'Digestelact'*
1*01
165
Australia
'Similac'
0
20
200
Australia
'Alfare'
1-85
315
Switzerland
'Enfalac
Premature'
2-17
335
Canada
'Nan'
0-34
345
Australia
'Portagen'*
6-25
935
United
States
'Infasoy'*
9-68
1335
Australia
'Glucose
Nutramigen'*
1149
1725
Australia
'Pregestimil'
11-80
1780
United
States
'Isomil'
3-74
1890
United
States
'Prosobee'
10-02
5030
Australia
*Samples
taken
from
different
batches.
tAluminium
content
in
1sg/g
(powder)
or
1Lg/ml
(liquid)
of
feed.
Mean
of
two
measurements
taken
on
separate
occasions.
tThe
calculated
aluminium
content
per
litre
of
feed
diluted
according
to
the
manufacturers'
recommendations
(to
20
kcaV30
ml)
with
water
assumed
to
contain
40
pg/litre
of
aluminium
(using the
measurements
in
column
1).
mode
with
no
background
correction
required.
Pyrolytic
furnace
tubes
were
used.
Contamination
was
controlled
by
ensuring
that
the
peak
height
absorbance
of
a
blank
firing
of
0-3%
hydrochloric
acid
did
not
exceed
0.02
units
relative
to
an
air
firing
yielding
a
visually
flat
baseline.
Results
The
results
are
shown
in
the
Table.
Fresh
breast
milk,
5%
glucose,
and
a
glucose-electrolyte
mixture
(both
prepared
in
the
formula
room
of
our
hospital)
were
found
to
have
similarly
low
concentrations
of
aluminium
comparable
with
known
hospital
tap
water
concentration.
Among
the
milk
feeds,
the
mean
concentration
of
aluminium
ranged
from
0-09
to
10-02
ig/ml
for
liquid
feeds
and
0-23
to
11-80
lAg/g
for
powdered
feeds.
Compared
with
a
litre
of
breast
milk
there
was
an
increase
of
up
to
165-fold
in
aluminium
content
per
litre
of
reconstituted
feed.
Depending
on
the
formula
used,
infants
drinking
a
litre
of
milk
daily
would
be
exposed
to
between
30
and
5000
,ug
of
aluminium
per
day.
Batch
to
batch
variation
and
country
of
origin
of
the
formulas
did
not
seem
to
influence
our
results.
Discussion
Aluminium
intoxication
is
now
recognised
as
the
cause
of
a
progressive
encephalopathy,
vitamin
D
resistant
osteomalacia,
and
one
form
of
anaemia
in
the
presence
of
chronic
renal
insufficiency.3
Although
these
manifestations
of
toxicity
were
initially
recognised
in
adults
with
uraemia
under-
going
haemodialysis,
they
were
subsequently
de-
scribed
in
children
who
were
receiving
large
doses
of
aluminium
containing
phosphate
binding
agents
but
who
did
not
yet
require
dialysis.5
Less
severe
forms
of
neurological
and
intellectual
dysfunction
in
infants
developing
chronic
renal
failure
in
the
first
year
of
life
are
well
known.
In
fact,
in
one
major
study
20
of
23
such
children
were
found
to
have
developmental
delay,
microcephaly,
hypotonia,
dyskinesia,
seizures,
and
electro-
encephalographic
abnormalities
on
subsequent
follow
up.6
Poor
nutrition,
raised
serum
parathyroid
hormone
concentration,
subsceptibility
of
the
infant
brain
to
the
uraemic
environment,
and
aluminium
toxicity
were
suggested
as
causes;6
the
possibility
that
the
aluminium
was
derived
from
infant
for-
mulas
was
not
considered.
More
recently,
cerebral
aluminium
accumulation
has
been
documented
in
two
infants
with
neonatal
uraemia
who
developed
a
progressive
and
fatal
encephalopathy
in
the
absence
of
phosphate
binding
gels
or
dialysis
with
water
appreciably
contaminated
with
aluminium.4
Both
infants
were
fed
with
a
proprietary
milk
formula
that
was
found
to
contain
high
concentrations
of
aluminium
relative
to
breast
milk.
Our
results
confirm
that
infants
may
be
exposed
916
Archives
of
Disease
in
Childhood,
1986,
61
to
appreciable
amounts
of
aluminium
from
a
variety
of
proprietary
milk
formulas,
some
of
which
contain
more
than
15
times
the
concentration
of
aluminium
already
implicated
in
cerebral
toxicity.4
This
source
of
exogenous
aluminium
may
contribute
to
other
recognised
forms
of
neurological
and
intellectual
dysfunction
in
infants
with
chronic
renal
insuf-
ficiency.
The
effects
of
exposure
to
large
quantities
of
ingested
aluminium
in
infants
with
lesser
degrees
of
renal
impairment
or
normal
renal
function
remain
to
be
documented.
By
comparison
with
phosphate
binding
gels,
the
total
aluminium
content
of
infant
milk
formulas
is
only
modest.
In
the
absence
of
other
commonly
recognised
risk
factors
cerebral
toxicity
may
there-
fore
reflect
a
greater
bioavailability
of
aluminium
in
milk
formulas
or
an
increased
uptake
of
aluminium
by
the
immature
brain.
The
authors
gratefully
acknowledge
the
cooperation
of
Sister
Barton-Bishop
for
her
help
with
the
feeds
and
Mrs
L
Beer
for
the
preparation
of
the
manuscript.
References
lGolden
MHN.
Trace
elements
in
human
nutrition.
Hum
Nutr
Clin
Nutr
1982;36:185-202.
2
Klein
GL,
Berquist
WE,
Ament
ME,
Coburn
JW,
Miller
NL,
Alfrey
AC.
Hepatic
aluminium
accumulation
in
children
on
total
parenteral
nutrition.
Journal
of
Pediatric
Gastroenterology
and
Nutrition
1984;3:740-3.
3Willis
MR,
Savory
J.
Aluminium
poisoning:
dialysis
encephalo-
pathy,
osteomalacia
and
anaemia.
Lancet
1983;ii:29-34.
4Freundlich
M,
Zilleruelo
G,
Abitbol
C,
Strauss
J.
Infant
formula
as
a
cause
of
aluminium
toxicity
in
neonatal
uraemia.
Lancet
1985;ii:527-9.
5Foley
CM,
Polinsky
MS,
Gruskin
AB,
Baluarte
NZ,
Grover
WD.
Encephalopathy
in
infants
and
children
with
chronic
renal
disease.
Arch
Neurol
1981;38:656-8.
6
Rotundo
A,
Nevins
TE,
Lipton
M,
Lockman
LA,
Mauer
SM,
Michael
AF.
Progressive
encephalopathy
in
children
with
chronic
renal
insufficiency
in
infancy.
Kidney
Int
1982;21:
486-91.
Correspondence
to
Dr
A
R
Rosenberg,
The
Prince
of
Wales
Children's
Hospital,
High
Street,
Randwick,
New
South
Wales
2031,
Australia.
Received
29
April
1986
... According to the study done by (Chuchu et al. 2013), they have measured the aluminum content of 30 different brands of milk formula, and all were aluminumbased packaging. Documentation of formulas with high contamination with aluminum is not a new topic, yet the values for aluminum content determined in the study done by Burrell and Exley (2010) do not significantly differ from values in older studies (Weintraub et al. 1986;Chedid et al. 1991). Burrell and Exley (2010) indicated that manufacturers are not really concerned with lowering the aluminum content in infant formula. ...
... Burrell and Exley (2010) indicated that manufacturers are not really concerned with lowering the aluminum content in infant formula. Weintraub et al. (1986) have measured the concentration of aluminum for different brands of milk formulas from different countries (Holland, Australia, Switzerland, Canada, and the USA). They found that the concentration of aluminum in infant formulas ranged from 85 up to 5000 μg/L. ...
... Hence, measuring the concentration of Al in antiperspirants and cosmetics and how much absorbed by the skin is of great necessity to ensure safe dermal use of these products. Unfortunately, there are only very few studies concerned with dermal exposure to Al (Corkins 2019;de Ligt et al. 2018;Freundlich et al. 1985;Weintraub et al. 1986). Guillard et al. (2004) have reported a case for a 43-year-old woman who experienced pain in her bones and excessive fatigue as a result of overexposure to Al from antiperspirant. ...
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... In recent years, several studies have provided scientific evidence that there is an association between aluminium exposure and Alzheimer's disease [84,85]. However,t he link between Alzheimer's disease and aluminium exposure from vaccination remains unclear,s ince aluminium uptake by food is much higher than by vaccination [61,86,87]. ...
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... Aluminium content in human milk and in infant formulas having much lower values of 27 ng/ml of milk has been reported in Koo et al. (1988), while concentrations ranging from 95 to 100 ng/ml have also been found in the USA (Andersson 1992), in Australia (Weintraub et al. 1986) and in Italy (de Curtis et al. 1989). On the contrary, much higher values (460 μg/l) were found by Abollino et al. (1998) in Torino (Italy) in semi-skimmed commercial milk, and especially in Anatolia (Turkey) with values much higher, ranging from 5650 to 8920 μg/kg of raw cow milk (Ayar et al. 2009). ...
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... This transports lead into the baby's blood stream [66], that otherwise would have passed on through without harm [161,167]. Infant formula is also commonly contaminated with aluminum, contributing an additional toxic burden [177][178][179]. The baby is also apt to be exposed to glyphosate from food sources routinely treated with the herbicide Roundup ® . ...
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Despite enjoying a high standard of living, the United States ranks 46th among nations reporting infant survival rates to the World Health Organization. Among factors that increase infant mortality are environmental toxicants. Toxic metals such as mercury, aluminum, and lead interact synergistically with uoride compounds to produce metal fuoride complexes (e.g., AlF3 and AlF4−). Such toxicants act as biophosphate mimetics disrupting biological signaling processes governing development, immune defenses, and ordinary maintenance systems. Sources for the metals include mother’s mercury amalgams, mercury and aluminum in injected medicines, and lead contaminated drinking water. All of them are made even more toxic by fuorides as evidenced recently by water contamination in Flint, Michigan. Fluorides interact with other toxins increasing their harmful impact. Among the interactants are glyphosate and phosphate containing fertilizers that end up in the food and water because of their widespread use in agriculture. The negative synergy for neonates in the U.S. is increased by the hepatitis B injection containing both mercury and aluminum, and infant formula contaminated with aluminum and the glyphosate in genetically modified soy milk reconstituted with water containing fluoride, aluminum, lead, and other toxic substances. The harmful interactions of such chemicals are associated with rising infant mortality in the U.S. We propose, therefore, a modest but urgent policy change: under TSCA §5, silicofluoride addition to public water supplies should be suspended.
... This transports lead into the baby's blood stream [66], that otherwise would have passed on through without harm [161,167]. Infant formula is also commonly contaminated with aluminum, contributing an additional toxic burden [177][178][179]. The baby is also apt to be exposed to glyphosate from food sources routinely treated with the herbicide Roundup ® . ...
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p>Despite enjoying a high standard of living, the United States ranks 46th among nations reporting infant survival rates to the World Health Organization. Among factors that increase infant mortality are environmental toxicants. Toxic metals such as mercury, aluminum, and lead interact synergistically with fluoride compounds to produce metal fluoride complexes (e.g., AlF3 and AlF4−). Such toxicants act as biophosphate mimetics disrupting biological signaling processes governing development, immune defenses, and ordinary maintenance systems. Sources for the metals include mother’s mercury amalgams, mercury and aluminum in injected medicines, and lead contaminated drinking water. All of them are made even more toxic by fluorides as evidenced recently by water contamination in Flint, Michigan. Fluorides interact with other toxins increasing their harmful impact. Among the interactants are glyphosate and phosphate containing fertilizers that end up in the food and water because of their widespread use in agriculture. The negative synergy for neonates in the U.S. is increased by the hepatitis B injection containing both mercury and aluminum, and infant formula contaminated with aluminum and the glyphosate in genetically modified soy milk reconstituted with water containing fluoride, aluminum, lead, and other toxic substances. The harmful interactions of such chemicals are associated with rising infant mortality in the U.S. We propose, therefore, a modest but urgent policy change: under TSCA §5, silicofluoride addition to public water supplies should be suspended. </p
... This transports lead into the baby's blood stream [66], that otherwise would have passed on through without harm [161,167]. Infant formula is also commonly contaminated with aluminum, contributing an additional toxic burden [177][178][179]. The baby is also apt to be exposed to glyphosate from food sources routinely treated with the herbicide Roundup ® . ...
Article
Full-text available
Despite enjoying a high standard of living, the United States ranks 46th among nations reporting infant survival rates to the World Health Organization. Among factors that increase infant mortality are environmental toxicants. Toxic metals such as mercury, aluminum, and lead interact synergistically with fluoride compounds to produce metal fluoride complexes (e.g., AlF3 and AlF4−). Such toxicants act as biophosphate mimetics disrupting biological signaling processes governing development, immune defenses, and ordinary maintenance systems. Sources for the metals include mother’s mercury amalgams, mercury and aluminum in injected medicines, and lead contaminated drinking water. All of them are made even more toxic by fluorides as evidenced recently by water contamination in Flint, Michigan. Fluorides interact with other toxins increasing their harmful impact. Among the interactants are glyphosate and phosphate containing fertilizers that end up in the food and water because of their widespread use in agriculture. The negative synergy for neonates in the U.S. is increased by the hepatitis B injection containing both mercury and aluminum, and infant formula contaminated with aluminum and the glyphosate in genetically modified soy milk reconstituted with water containing fluoride, aluminum, lead, and other toxic substances. The harmful interactions of such chemicals are associated with rising infant mortality in the U.S. We propose, therefore, a modest but urgent policy change: under TSCA §5, silicofluoride addition to public water supplies should be suspended.
Article
Background Aluminum toxicity is well documented and contamination of milk formulas has been implicated as the source of accumulation in bone and brain tissues. The purpose of the current study was to evaluate the aluminum contents of human milk, cow's milk, and infant formulas. Methods Aluminum contents were determined by atomic absorption spectrometry in samples of human milk in the colostrum, intermediate, and mature stages; infant formulas from eight manufacturers; and various types and brands of commercially available cow's milk. Results Mean aluminum concentration was lowest in human milk (23.4 ± 9.6 µg/l), and did not differ significantly between colostrum, intermediate‐stage and mature‐stage milk. Mean aluminum concentration was 70 µg/l in cow's milk, and 226 µg/l in reconstituted infant formulas. Aluminum concentrations in infant formulas differed markedly among manufacturers; concentration in milk from one of the manufacturers was particularly high (mean, 551 µg/l; range, 302‐1149 µg/l). These values are for milk reconstituted with aluminum‐free water under laboratory conditions; formulas prepared with tap water in the University Hospital's infant‐feeding unit had even higher aluminum content. Experiments showed that aluminum concentration in the high‐aluminum milk could be reduced by more than 70% at the manufacturing stage, by using low‐aluminum components. Conclusions The results of the present study support the recommendations for infant formula manufacturers to strive to reduce aluminum concentration in their products.
Article
Background: Aluminum exposure may originate from numerous sources, including antiperspirants. Aluminum toxicity can cause a wide range of neurological impairments. Infants are exposed to aluminum through human milk (HM), formulas, total-parenteral-nutrition and vaccines. Due to potential risk of toxicity to both infants and women, it has been advised that lactating women decrease their use of aluminum-based products and antiperspirants. Our study aimed to determine whether the use of aluminum-based antiperspirants (ABA) affects aluminum levels in HM. Methods: This cross-sectional study included healthy mothers who exclusively breastfed infants (1 week to 5 months). Questionnaires were used to collect data on demographics, antiperspirant use and aluminum exposure. Mothers were instructed to express HM during the morning at first breastfeeding session. Aluminum levels were measured by atomic absorption spectrometry with a 5 ppb limit of detection. Results: Fifteen of the 58 (26%) recruited mothers used an aluminum-free antiperspirant (AFA) and 43 (74%) used an ABA. The range of aluminum concentration in HM was 0-100.8 μg/L (mean 11.4 ± 17.4 μg/L). The median aluminum level (Q1-Q3) was 6.5 μg/L (5.2-11.9) and 5.2 μg/L (3.46-9.4) in the AFA and ABA groups, respectively (p = 0.19). The aluminum levels were not affected by maternal age, education, diet, number of children, infant age, lactation stage or self-reported aluminum exposure. Conclusion: The data from this preliminary study demonstrate that the use of an ABA by lactating mothers does not increase their HM aluminum content. Additional studies with a larger cohort are warranted to confirm these findings.
Article
Backgroung Exposure to environmental pollutants in critical developmental windows may predispose the prostate to permanent changes in its homeostasis. Thus, it is essential to know the effects that environmental toxics, such as aluminum, can cause during the development of this gland. The aim of this study was to evaluate the effects of neonatal aluminum exposure on the ventral male prostate and the female prostate of 15 days old gerbils. Methods Male and female gerbils were exposed orally to 10 mg/kg/day of aluminum chloride from the 1st to the 14th postnatal day life. At 15 days of life, gerbils were euthanized and their prostates were collected for biometric, morphological, morphometric, immunohistochemical and three-dimensional reconstruction analyzes. Results Al exposure caused a reduction in body weight in males and a significant increase in serum testosterone levels in females. Prostate branching morphogenesis was intensified in males, who had greater length, number and area of prostatic epithelial buds. Additionally, Al altered the prostate hormonal regulation of males and females, causing up regulation of the androgen receptor and estrogen receptor alpha in the female prostate, and increased immunostaining of the androgen receptor in the ventral male prostate. These changes were associated with an increased rate of epithelial and stromal cell proliferation in both sexes. Conclusion Together, these results indicate that Al altered the neonatal development of the prostate and that this metal acted as an endocrine disruptor in this gland.
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Article
Aluminium toxicity occurred in two infants with congenital uraemia who had never received phosphate binders or other aluminium-containing agents or intravenous fluids. One patient was treated by peritoneal dialysis from the age of two weeks and died at three months after the sudden onset of neurological symptoms; the other died after one month of conservative management without dialysis. Brain aluminium concentration was high in both infants (6.4 and 47 micrograms/g, respectively) whereas bone aluminium content was normal and there were no histological changes or stainable aluminium on bone biopsy specimens. Both infants were fed with 'Similac PM 60/40'. To investigate possible sources of aluminium, powdered milk formula, sterilised water used for preparation of the feed, and dialysate concentrate (first patient) were analysed. Aluminium concentration was high (232 +/- 60 ng/ml) in powdered milk but negligible in sterilised water and dialysate concentrate (4 ng/ml and 3.4 +/- 2.4 ng/ml, respectively). These findings indicate that proprietary infant milk formula is another source of aluminium. Aluminium-free milk should contribute to the prevention of aluminium toxicity in infants with renal failure.
Article
Five children receiving long-term total parenteral nutrition (TPN) containing casein hydrolysate as the protein source underwent percutaneous liver biopsies because of the development of cholestasis and abnormal liver function tests. All five demonstrated moderate to severe histopathologic changes. In addition, hepatic aluminum content was determined to be markedly elevated in all cases. Although the hepatotoxicity of aluminum is as yet undetermined, deposition of other metals has been associated with liver damage, and aluminum has been associated with pathology in other tissues. Thus, the possibility that aluminum deposition may play a role in the pathogenesis or exacerbate the course of liver dysfunction associated with TPN should be considered.
Article
Progressive encephalopathy in children with chronic renal insufficiency in infancy. A retrospective analysis of children with renal failure during the first year of life revealed that 20 of 23 patients developed profound neurologic abnormalities. The encephalopathy was characterized by developmental delay, microcephaly, hypotonia, seizures, dyskinesia, and EEG abnormalities. No patient had been dialyzed, and four had not received aluminum salts prior to the development of neurologic symptoms. Inadequate statural growth and poor nutrition were present in all patients. It is probable that infants with chronic renal insufficiency are more susceptible to the development of this syndrome than are older children or adults because of the significant growth and maturation of the brain that occurs during the first years of life. Encéphalopathie progressive chez des enfants atteints d'insuffisance rénale chronique au cours de la petite enfance. Une analyse rétrospective réalisée chez des enfants ayant eu une insuffisance rénale au cours de la première année de leur vie a montré que 20 sur les 23 malades étudiés ont développé des anomalies neurologiques importantes. L'encéphalopathie est caractérisée par un retard de développement, une microcéphalie, une hypotonie, des crises convulsives, une dyskynésie, des anomalies électroencéphalographiques. Aucun de ces malades n'avait été en dialyse et 4 d'entre eux n'avaient pas reçu de sels d'aluminium avant l'apparition des signes neurologiques. Une croissance staturale insuffisante et un mauvais état nutritionnel ont été constatés chez tous les malades. Il est probable que les enfants atteints d'insuffisance rénale chronique sont plus exposés au développement de ce syndrome que des enfants plus âgés ou des adultes en raison de la croissance et de la maturation importantes qui affectent le cerveau au cours des premières années de la vie.
Article
The examination of five pediatric patients with encephalopathy secondary to chronic renal failure has indicated a stereotyped sequence of neurologic signs and symptoms including ataxia, loss of motor abilities, myoclonus, seizures, dementia, and bulbar dysfunction. Both the patients with CNS dysfunction and a control group selected for a similar degree of renal failure had increased levels of serum phosphate, alkaline phosphatase, and parathyroid hormone. Serial EEGs in the affected group revealed progressive slowing and an increase in paroxysmal features. No specific neuropathologic findings were noted in one patient.
The Prince of Wales Children's Hospital, High Street
  • Correspondence To Dr
  • A Rosenberg
Correspondence to Dr A R Rosenberg, The Prince of Wales Children's Hospital, High Street, Randwick, New South Wales 2031, Australia.
Aluminium poisoning: dialysis encephalopathy , osteomalacia and anaemia Infant formula as a cause of aluminium toxicity in neonatal uraemia Encephalopathy in infants and children with chronic renal disease
  • Mr Savory
  • M Zilleruelo
  • G Abitbol
  • C Strauss
  • J Polinsky
  • Ms Gruskin
  • Ab Baluarte
  • Nz Grover
3Willis MR, Savory J. Aluminium poisoning: dialysis encephalopathy, osteomalacia and anaemia. Lancet 1983;ii:29-34. 4Freundlich M, Zilleruelo G, Abitbol C, Strauss J. Infant formula as a cause of aluminium toxicity in neonatal uraemia. Lancet 1985;ii:527-9. 5Foley CM, Polinsky MS, Gruskin AB, Baluarte NZ, Grover WD. Encephalopathy in infants and children with chronic renal disease. Arch Neurol 1981;38:656-8.
elements in human nutrition
elements in human nutrition. Hum Nutr Clin Nutr 1982;36:185-202.
The Prince of Wales Children's Hospital
  • Correspondence To Dr A R Rosenberg
Correspondence to Dr A R Rosenberg, The Prince of Wales Children's Hospital, High Street, Randwick, New South Wales 2031, Australia.