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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