Document ID: EPA-HQ-OW-2002-0021-0137
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2003-05-15T04:00Z

Drinking
Water
Advisory:
Consumer
Acceptability
Advice
and
Health
Effects
Analysis
on
Sodium
Printed
on
Recycled
Paper
Drinking
Water
Advisory:
Consumer
Acceptability
Advice
and
Health
Effects
Analysis
on
Sodium
Prepared
for:

U.
S.
Environmental
Protection
Agency
Office
of
Water
(
4304T)
Health
and
Ecological
Criteria
Division
Washington,
DC
20460
www.
epa.
gov/
safewater/
ccl/
pdf/
sodium.
pdf
EPA
822­
R­
03­
006
February
2003
iii
FOREWORD
The
Drinking
Water
Advisory
Program
sponsored
by
the
Health
and
Ecological
Criteria
Division
of
the
Office
of
Science
and
Technology
(
OST),
Office
of
Water
(
OW),
provides
information
on
the
health
and
organoleptic
(
taste,
odor,
etc.)
effects
of
contaminants
in
drinking
water.
The
Drinking
Water
Advisory
documents
are
a
component
of
the
OW
Health
Advisory
program.
Drinking
Water
Advisories
differ
from
Health
Advisories
because
of
their
focus
on
esthetic
properties
(
taste,
odor,
color)
of
drinking
water.
A
Drinking
Water
Advisory
is
prepared
when
the
adverse
contaminants
cause
adverse
taste
and
odor
influences
at
concentrations
lower
than
those
for
possible
health
effects.

A
Drinking
Water
Advisory
is
not
an
enforceable
standard
for
action.
However,
it
describes
nonregulatory
concentrations
of
the
contaminant
in
water
that
are
expected
to
be
without
adverse
effects
on
both
health
and
esthetics.
Both
Health
Advisories
and
Drinking
Water
Advisories
serve
as
informal
technical
guidance
to
assist
Federal,
State
and
local
officials
responsible
for
protecting
public
health
when
emergency
spills
or
contamination
situations
occur.
They
are
not
to
be
construed
as
legally
enforceable
Federal
standards.
They
are
subject
to
change
as
new
information
becomes
available.
This
draft
supersedes
any
previous
draft
advisories
for
this
chemical.

The
Advisory
discusses
the
limitations
of
the
current
database
for
estimating
a
risk
level
for
sodium
in
drinking
water
and
characterizes
the
hazards
associated
with
exposure.
The
document
was
peer
reviewed
internally
and
externally
by
experts
in
the
field.
External
peer
reviewers
were
as
follows:

Paul
E.
Brubaker,
Ph.
D.
 
Brubaker
Associates,
New
Jersey
Janet
L.
Greger,
Ph.
D.
 
University
of
Wisconsin
­
Madison
(
Nutritional
Science
Department
and
Environmental
Toxicology
Program)
Jeanne
Freeland­
Graves,
Ph.
D.
 
The
University
of
Texas
at
Austin
(
Nutritional
Sciences)
iv
Sodium
 
February
2003
TABLE
OF
CONTENTS
Executive
Summary
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1
1.0
Introduction
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4
2.0
Sodium
in
the
Environment
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4
2.1
Air
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4
2.2
Soil
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4
2.3
Water
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4
2.4
Food
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6
3.0
Chemical
and
Physical
Properties
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6
4.0
Toxicokinetics
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6
4.1
Absorption
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8
4.2
Distribution
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8
4.3
Metabolism
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8
4.4
Excretion
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8
5.0
Health
Effects
Data
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9
5.1
Humans
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9
5.1.1
Short­
Term
Exposure
Studies
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9
5.1.2
Long­
Term
Exposure
Studies
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10
5.1.3
Sensitive
Populations
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14
5.2
Animal
Studies
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15
5.2.1
Short­
Term
Exposure
Studies
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15
5.2.2
Long­
Term
Exposure
Studies
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15
5.2.3
Reproductive
Studies
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15
5.2.4
Developmental
Studies
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16
5.2.5
Genotoxicity
Studies
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16
5.2.6
Cancer
Studies
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16
6.0
Organoleptic
Properties
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17
7.0
Characterization
of
Hazard
and
Dose­
Response
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19
7.1
Hazard
Characterization
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19
7.2
Characterization
of
Organoleptic
Effects
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21
7.3
Dose­
Response
Characterization
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21
8.0
References
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23
v
Sodium
 
February
2003
LIST
OF
ABBREVIATIONS
g
gram
Hg
mercury
kg
kilogram
L
liter
mg
milligram
mm
millimeter
mM
millimolar
mEq
milliequivalents
mmol
millimole
NAS
National
Academy
of
Sciences
Na+
sodium
ion
ppm
parts
per
million
1
Sodium
 
February
2003
DRINKING
WATER
ADVISORY:
CONSUMER
ACCEPTABILITY
ADVICE
AND
HEALTH
EFFECTS
ANALYSIS
ON
SODIUM
Executive
Summary
The
EPA
Office
of
Water
is
issuing
this
Drinking
Water
Advisory
to
provide
guidance
to
communities
that
may
be
exposed
to
drinking
water
containing
sodium
chloride
or
other
sodium
salts.
The
Advisory
provides
a
summary
of
the
current
health
hazard
information
and
an
evaluation
of
available
data
on
taste
problems
associated
with
sodium
in
drinking
water.
This
Advisory
does
not
recommend
a
reference
dose
because
data
for
quantifying
risk
are
limited.
The
Advisory
provides
guidance
on
concentrations
at
which
problems
with
taste
would
likely
occur.

EPA
requires
periodic
monitoring
of
sodium
at
the
entry
point
to
the
distribution
system.
Monitoring
is
to
be
conducted
annually
for
surface
water
systems
and
every
3
years
for
groundwater
systems
(
40
CFR:
141.41).
The
water
supplier
must
report
sodium
test
results
to
local
and
State
public
health
officials
by
direct
mail
within
3
months
of
the
analysis,
unless
this
responsibility
is
assumed
by
the
State.
This
provides
the
public
health
community
with
information
on
sodium
levels
in
drinking
water.

Conclusion
and
Recommendation
This
Advisory
recommends
reducing
sodium
concentrations
in
drinking
water
to
between
30
and
60
mg/
L
based
on
esthetic
effects
(
i.
e.,
taste).
This
recommendation
is
not
federally
enforceable
but
is
intended
as
a
guideline
for
States.
States
may
establish
higher
or
lower
levels
depending
on
local
conditions,
such
as
unavailability
of
alternate
source
waters
or
other
compelling
factors,
provided
that
public
health
and
welfare
are
not
adversely
affected.
A
goal
of
2.4
g/
day
dietary
sodium
has
been
proposed
by
several
government
and
health
agencies.
Drinking
water
containing
between
30
and
60
mg/
L
is
unlikely
to
be
perceived
as
salty
by
most
individuals
and
would
contribute
only
2.5%
to
5%
of
the
dietary
goal
if
tap
water
consumption
is
2
L/
day.

At
the
present
time
the
EPA
guidance
level
for
sodium
in
drinking
water
is
20
mg/
L.
This
value
was
developed
for
those
individuals
restricted
to
a
total
sodium
intake
of
500
mg/
day
and
should
not
be
extrapolated
to
the
entire
population
Sodium
in
the
Environment
Sodium
is
the
sixth
most
abundant
element
on
Earth
and
is
widely
distributed
in
soils,
plants,
water,
and
foods.
Most
of
the
world
has
significant
deposits
of
sodium­
containing
minerals.
Sodium
ion
is
ubiquitous
in
water
because
of
the
high
solubility
of
many
sodium
salts.
Groundwater
typically
contains
higher
concentrations
of
minerals
and
salts
than
do
surface
waters.
Sodium
is
present
in
road
deicing
chemicals,
in
water
treatment
chemicals,
in
domestic
water
softeners,
and
in
sewage
effluents.
These
uses
contribute
significant
quantities
of
sodium
to
water.
2
Sodium
 
February
2003
Sodium
is
a
normal
component
of
the
body,
and
adequate
levels
of
sodium
are
required
for
good
health.
Food
is
the
main
source
of
daily
human
exposure
to
sodium,
primarily
in
the
form
of
sodium
chloride
(
salt).
Most
of
the
sodium
in
our
diet
is
added
to
food
during
processing
and
preparation.
Various
studies
have
reported
that
dietary
intakes
of
sodium
range
from
1,800
to
5,000
milligrams
per
day
(
mg/
day),
depending
on
methods
of
assessment
and
on
whether
discretionary
sodium
use
is
assessed.
Discretionary
sodium
intake
is
variable
and
can
be
quite
large.
The
Food
and
Drug
Administration
has
found
that
most
American
adults
tend
to
consume
between
4,000
and
6,000
mg
of
sodium/
day,
and
therapeutic
sodium­
restricted
diets
can
range
from
below
1,000
to
3,000
mg/
day.

Studies
of
Sodium
Effects
Cancer
Studies.
Ingestion
of
sodium
ion
is
not
believed
to
cause
cancer.
However,
some
studies
suggest
that
sodium
chloride
may
enhance
cancer
risk
caused
by
other
chemicals
in
the
gastrointestinal
tract.
Sodium
salts
have
generally
produced
inconclusive
or
negative
results
in
in
vitro
or
in
vivo
genotoxicity
tests.

Noncancer
Studies.
Very
high
oral
doses
of
sodium
chloride
may
cause
nausea,
vomiting,
inflammation
of
the
gastrointestinal
tract,
thirst,
muscular
twitching,
convulsions,
and
possibly
death.
For
long­
term,
lower
level
exposures,
the
primary
health
effect
of
concern
is
increased
blood
pressure
(
hypertension).
A
large
body
of
evidence
suggests
that
excessive
sodium
intake
contributes
to
age­
related
increases
in
blood
pressure
leading
to
hypertension.
Increased
blood
pressure
has
also
been
clearly
demonstrated
in
several
animal
species
given
high
concentrations
of
sodium
chloride
in
their
diets.

High
doses
of
sodium
chloride
(
about
1,570
mg
sodium/
kg
body
weight)
have
been
observed
to
cause
reproductive
effects
in
various
strains
of
pregnant
rats.
Effects
on
the
dams
have
included
decreases
in
pregnancy
rates
and
maternal
body
weight
gain.
Developmental
effects
have
included
increased
blood
pressure
and
high
mortality.
However,
these
effects
were
observed
only
in
SHR
rat
pups
(
a
type
of
rat
specifically
bred
to
be
hypertensive)
fed
high
sodium
diets
for
up
to
4
months
after
parturition.
This
study
reported
no
developmental
effects
in
Sprague­
Dawley
or
WKY
rat
pups
(
both
normotensive
strains).
Developmental
effects
have
not
been
studied
in
other
species.

Studies
on
Taste
and
Odor.
Several
studies
are
available
on
the
taste
threshold
of
sodium
chloride
in
drinking
water.
It
is
not
possible
to
identify
precise
threshold
values
for
the
taste
of
sodium
in
drinking
water
because
detectable
concentrations
vary
among
individuals
and
for
the
same
individuals
at
different
times.
Age
and
health
status
also
impact
a
person's
ability
to
detect
the
taste
of
sodium.
Other
factors
affecting
taste
of
sodium
in
drinking
water
include
possible
masking
by
other
dissolved
substances,
water
temperature,
and
the
anion
forming
the
salt.
The
average
taste
threshold
for
sodium
in
water
at
room
temperature
differs
substantially
among
individuals
and
ranges
from
about
30
mg/
L
to
460
mg/
L.
Sodium
in
water
does
not
by
itself
cause
odor
problems.
The
World
Health
Organization
has
established
a
drinking
water
guideline
of
200
mg
of
sodium/
L
on
the
basis
of
esthetic
considerations
(
i.
e.,
taste).
When
sodium
chloride
is
dissolved
in
distilled
water,
it
is
possible
to
detect
the
overall
impact
on
taste
prior
to
recognition
of
the
taste
as
salty.
3
Sodium
 
February
2003
Characterization
Summary.
Although
numerous
human
studies
have
examined
the
relationship
between
sodium
intake
and
blood
pressure,
these
studies
are
not
suitable
for
defining
a
quantitative
dose­
response
relationship
because
(
1)
the
dose­
response
relationships
varied
among
the
different
studies,
(
2)
sodium
intake
measurements
were
generally
indirect
(
determined
by
the
amount
of
sodium
excreted
in
the
urine),
and
(
3)
the
results
may
have
been
influenced
by
nutrients
in
the
diet
other
than
sodium,
by
lifestyle,
and
by
patterns
of
behavior.

Drinking
water
does
not
play
a
significant
role
in
sodium
exposure
for
most
individuals.
Those
that
are
under
treatment
for
sodium­
sensitive
hypertension
should
consult
with
their
health
care
provider
regarding
sodium
levels
in
their
drinking
water
supply
and
the
advisability
of
using
an
alternative
water
source
or
point­
of­
use
treatment
to
reduce
the
sodium.
For
individuals
on
a
very
low
sodium
diet
(
500
mg/
day),
EPA
recommends
that
drinking­
water
sodium
not
exceed
20
mg/
L.
In
order
to
avoid
adverse
effects
on
taste,
EPA
recommends
that
sodium
concentrations
in
drinking
water
not
exceed
30
to
60
mg/
L,
a
threshold
for
taste­
sensitive
segments
of
the
population.
Many
individuals
will
not
be
able
to
detect
the
presence
of
sodium
in
this
concentration
range.

EPA
requires
periodic
monitoring
of
sodium
at
the
entry
point
to
the
distribution
system.
Monitoring
is
to
be
conducted
annually
for
surface
water
systems
and
every
3
years
for
groundwater
systems
(
40CFR:
141.41).
The
water
supplier
must
report
sodium
test
results
to
local
and
State
public
health
officials
by
direct
mail
within
3
months
of
the
analysis,
unless
this
responsibility
is
assumed
by
the
State.
This
provides
the
public
health
community
with
information
on
sodium
levels
in
drinking
water.
4
Sodium
 
February
2003
1.0
INTRODUCTION
The
purpose
of
this
Advisory
is
to
provide
information
to
States,
local
drinking
water
facilities,
and
public
health
personnel
on
the
potential
health
and
esthetic
effects
resulting
from
ingestion
of
sodium­
containing
potable
water,
as
well
as
on
the
concentrations
of
sodium
that
are
typically
found
in
water.

2.0
SODIUM
IN
THE
ENVIRONMENT
Sodium
is
a
common
element
in
the
environment
and
occurs
widely
in
soils,
plants,
water,
and
foods.
Sodium
chloride
is
the
most
economically
and
industrially
important
form
of
sodium,
with
an
estimated
14,000
direct
and
indirect
uses
(
Kostick
1993).
Sodium
chloride
use
can
be
broken
down
into
eight
major
categories:
chemical
(
47%),
ice
control
(
25%),
food
processing
(
5%),
general
industrial
(
5%),
agricultural
(
5%),
distributors
(
5%),
water
treatment
(
4%),
and
miscellaneous
(
4%).
Other
sodium
salts
are
used
in
personal
care
products,
foods,
nutritional
supplements,
and
medications.

2.1
Air
Sodium
salts
are
nonvolatile,
and
sodium
does
not
occur
in
air
except
in
association
with
suspended
particulate
matter
or
water
droplets.
Because
sodium
is
nonvolatile,
the
concentrations
of
sodium
salts
in
air
are
usually
low,
especially
in
comparison
to
the
concentrations
of
sodium
typically
found
in
water
or
soil.
Ambient
air
concentrations
in
coastal
areas
may
be
higher
than
for
inland
areas
because
of
ocean
spray
droplets
introduced
into
the
atmosphere.

2.2
Soil
Sodium
is
the
sixth
most
abundant
element
on
Earth,
making
up
about
2.6%
of
the
Earth's
crust.
Sodium
concentrations
in
soil
and
other
surficial
materials
of
the
conterminous
United
States
range
widely,
from
less
than
500
parts
per
million
(
ppm
or
mg/
kg)
to
more
than
100,000
ppm
(
Shacklette
and
Boerngen
1984).
Sodium
is
also
transported
from
the
ocean
to
the
atmosphere
by
spray
and
is
suspended
in
water
droplets
until
it
is
either
precipitated
or
introduced
to
the
soil
by
dry
deposition
(
Fairbridge
1972).
The
application
of
fertilizers
and
other
agricultural
products
that
contain
sodium
salts
can
increase
the
sodium
in
soils.

2.3
Water
Sodium
ion
is
ubiquitous
in
water,
owing
to
the
high
solubility
of
its
salts
and
the
abundance
of
sodium­
containing
mineral
deposits.
Seawater
contains
about
30,000
mg
of
sodium
chloride
per
liter
(
mg/
L).
Sodium
chloride
can
also
be
found
in
many
rivers
and
inland
lakes
and
seas,
in
concentrations
varying
from
20
mg/
L
in
the
Mississippi
River
to
120,000
mg/
L
in
the
Great
Salt
Lake
(
Chemistry
Explorer
2000).
Groundwater
typically
contains
higher
concentrations
of
minerals
and
salts
than
surface
waters,
especially
in
areas
with
an
abundance
of
sodium
mineral
deposits
or
in
areas
with
sea
or
estuarine
water
intrusions
(
WHO
1979).
5
Sodium
 
February
2003
There
are
a
number
of
anthropogenic
sources
of
sodium
that
can
contribute
significant
quantities
of
sodium
to
surface
water,
including
road
salt,
water
treatment
chemicals,
domestic
water
softeners,
and
sewage
effluents.
Water
treatment
chemicals
such
as
sodium
fluoride,
sodium
silicofluoride,
sodium
hydroxide,
sodium
carbonate,
sodium
bicarbonate,
sodium
phosphate,
sodium
silicate,
and
sodium
hypochlorite
provide
a
relatively
small
contribution
when
used
individually,
but
when
used
together
may
result
in
concentrations
of
up
to
30
mg/
L
(
WHO
1979).

The
addition
of
sodium
compounds
during
water
treatment
for
adjustment
of
pH
and
water
softening
are
the
uses
most
likely
to
increase
the
sodium
content
of
drinking
water.
Sodium
hydroxide,
sodium
carbonate,
and
sodium
bicarbonate
are
used
for
pH
adjustment
and
can
contribute
from
27
to
57
mg/
L
sodium
to
water
at
their
approved
maximum
use
levels
(
NSF
1997).
Domestic
water
softeners
can
increase
sodium
levels
to
more
than
300
mg/
L
in
drinking
water
(
NAS
1977).

Salt
that
has
been
used
to
deice
roads
can
also
be
a
problem
for
drinking
water
systems.
Salt
mixed
with
ice
dissolves
and
creates
a
brine
with
a
lower
freezing
point
than
water,
effectively
melting
ice
(
Kostick
1993).
Salt
is
a
cheap
and
effective
solution
to
ice­
covered
roads,
but
can
become
an
environmental
concern
as
runoff
that
affects
local
vegetation
and
soil
quality,
as
well
as
groundwater
and
surface
water
supplies.

The
National
Inorganic
and
Radionuclide
Survey
(
NIRS)
collected
national
occurrence
data
on
selected
radionuclides
and
inorganic
chemicals
in
drinking
water.
The
NIRS
investigated
989
community
public
water
supplies
(
PWSs)
served
by
groundwater
(
Cadmus
2001).
The
PWSs
selected
were
statistically
representative
of
national
occurrence.
Almost
100%
of
the
PWSs
were
found
to
have
detectable
levels
of
sodium:
37%
had
sodium
levels
greater
than
30
mg/
L
and
served
approximately
28
million
people;
13%
had
sodium
levels
greater
than
120
mg/
L
and
served
approximately
7.1
million
people.
The
median
concentration
for
all
samples
was
16.4
mg/
L
and
the
99th
percentile
was
517
mg/
L.
The
99th
percentile
concentration
is
a
summary
statistic
to
indicate
the
upper
bound
of
occurrence
values
because
maximum
values
can
be
extreme
values
(
outliers)
that
sometimes
result
from
sampling
or
reporting
error.

One
limitation
of
the
NIRS
study
is
a
lack
of
occurrence
data
for
surface
water
systems.
To
better
understand
the
occurrence
of
sodium
in
surface
water,
occurrence
data
from
Safe
Drinking
Water
Act
(
SDWA)
compliance
monitoring
were
reviewed
from
States
with
both
surface
and
groundwater
systems
(
Cadmus
2001).
Only
Alabama,
California,
Illinois,
New
Jersey,
and
Oregon
had
occurrence
data
for
sodium.
The
data
represent
analytical
samples
from
more
than
5,500
PWSs.
Sodium
was
detected
in
99.3%
to
100%
of
groundwater
PWSs
and
in
100%
of
surface
water
PWSs.
The
median
and
99th
percentile
concentrations
(
for
both
groundwater
and
surface
water
PWSs)
ranged
from
5.26
to
31
mg/
L
and
from
150
to
370
mg/
L,
respectively.
For
the
five
States,
the
percentage
of
PWSs
with
sodium
detected
in
surface
water
at
concentrations
greater
than
30
or
120
mg/
L
was
generally
lower
than
for
groundwater
systems.
6
Sodium
 
February
2003
2.4
Food
Foods
and
beverages
are
the
largest
sources
of
sodium
intake
for
humans.
Of
the
sodium
present
in
foods,
a
relatively
low
amount
(
10%)
occurs
naturally
(
Sanchez­
Castillo
et
al.
1987a,
b).
The
majority
of
dietary
sodium
comes
from
sodium
chloride
added
to
food
during
food
processing
and
preparation.
For
example,
Sanchez­
Castillo
et
al.
(
1987a,
b)
estimated
that
15%
of
dietary
sodium
comes
from
salt
added
during
cooking
and
at
the
table,
and
75%
comes
from
salt
added
during
processing
and
manufacturing.
The
first
National
Health
and
Nutrition
Examination
Survey
(
Abraham
and
Carroll
1981)
reported
that
approximately
32%
of
the
sodium
chloride
consumed
came
from
baked
goods
and
cereals,
21%
came
from
meats,
and
14%
from
dairy
products.
Similar
results
were
reported
for
the
FDA
Total
Diet
Study
(
Pennington
et
al.
1984).
Using
data
from
the
1989
to
1991
Continuing
Survey
of
Food
Intake
by
Individuals,
Subar
et
al.
(
1998)
found
that
23.4%
of
the
salt
in
the
diet
came
from
a
group
of
foods
that
included
cold
cuts
and
other
processed
meats,
condiments,
snack­
type
foods
(
e.
g.,
chips
and
popcorn),
and
table
salt;
10.9%
from
yeast
bread;
5.6%
from
cheese;
and
4.1%
from
ham.
These
foods
contributed
44.1%
of
the
total
dietary
sodium.

Reported
dietary
sodium
intakes
range
from
1,800
mg/
day
to
5,000
mg/
day
in
various
studies,
depending
on
the
methods
of
assessment
and
whether
discretionary
sodium
use
is
assessed
(
Abraham
and
Carroll
1981,
Pennington
et
al.
1984,
Karanja
et
al.
1999).
Discretionary
sodium
intake
is
highly
variable
and
can
be
quite
large.
In
a
28­
day
study,
Mickelson
et
al.
(
1977)
found
that
males
added
an
average
of
about
5,500
mg
of
sodium
chloride
(
2,200
mg
of
sodium)
to
their
food
per
day.
The
Food
and
Drug
Administration
has
found
that
most
American
adults
tend
to
consume
between
4,000
and
6,000
mg
of
sodium
per
day,
whereas
individuals
on
sodiumrestricted
diets
usually
ingest
less
than
1,000
to
3,000
mg/
day
(
Kurtzweil
1995).

3.0
CHEMICAL
AND
PHYSICAL
PROPERTIES
Sodium
(
Na)
is
the
most
abundant
element
of
the
alkali
metal
group.
Elemental
sodium
has
an
atomic
weight
of
22.99
and
is
a
soft,
bright
silvery
metal.
Pure
metallic
sodium
is
highly
reactive
and
burns
in
air
to
form
sodium
oxide,
which
in
turn
readily
hydrolyzes
in
water
to
form
sodium
hydroxide.
Because
elemental
sodium
is
so
highly
reactive,
it
is
not
found
freely
in
nature.
Rather,
sodium
is
found
in
nature
only
as
the
sodium
ion
(
Na+)
combined
with
a
variety
of
anions
to
form
a
number
of
different
salts.
Common
sodium
salts
are
chloride,
carbonate,
hypochlorite,
and
silicate.
The
physical
and
chemical
properties
of
five
sodium
salts
are
presented
in
Table
3
 
1
(
Sax
1975,
Clayton
and
Clayton
1981,
Sittig
1981,
Sax
and
Lewis
1987,
Budavari
1996,
HSDB
2000).

4.0
TOXICOKINETICS
Sodium
ions
are
a
normal
and
essential
component
of
the
human
body,
playing
a
key
role
in
controlling
and
maintaining
the
proper
osmolarity
(
concentration)
and
volume
of
extracellular
body
fluids.
Both
the
body
content
of
sodium
and
its
concentration
in
body
fluids
are
under
homeostatic
control.
In
addition
to
its
role
in
regulating
osmolarity
and
extracellular
fluid
volume,
sodium
is
important
in
the
regulation
of
acid­
base
balance
and
the
membrane
potential
of
cells.
As
a
consequence
of
these
vital
functions,
the
absorption,
distribution,
and
excretion
of
7
Table
3­
1.
Physical
and
Chemical
Properties
of
Sodium
and
Sodium
Salts
Chemical
Name
Sodium
Sodium
Chloride
Sodium
Carbonate
Sodium
Hypochlorite
Sodium
Silicate
Sodium
Sulfate
CAS
Number
7440­
23­
5
7647­
14­
5
497­
19­
8
7681­
52­
9
1344­
09­
8
7757­
82­
6
Chemical
Formula
Na
NaCl
Na
2
CO
3
NaOCl
Na
2
SiO
3
Na
2
SO
4
Molecular
Weight
22.99
58.44
105.99
74.44
99.07
142.06
Physical
State
Silver
metal
Colorless
cubic
crystal
or
white
crystalline
powder
White
powder
In
solution
only
Colorless
crystal
White
powder
or
orthorhombic
bipyramidal
crystals
Boiling
Point
(
oC)
881.4
1,413
Decomposes
 
 
 
Melting
Point
(
oC)
97.83
801
851
 
 
888
Density
(
g/
mL)
(
20oC)
0.71
2.17
2.53
 
 
2.67
Vapor
Pressure
(
mm
Hg)
1
 
 
 
 
 
Specific
Gravity
0.71
2.17
2.53
 
 
2.67
Water
Solubility
(
g/
100
mL)
React
violently
35.7
7.1
Infinitely
soluble
Slightly
soluble
or
almost
insoluble
in
cold
water.
Soluble
in
about
3.6
parts
water.
Max.

solubility
at
33
°
:

1
in
2
Taste
Threshold
(
Water)

(
mg/
L)
 
30
­
460
See
Section
6.0
 
 
 
180
­
550
8
Sodium
 
February
2003
sodium
ion
has
been
extensively
studied
in
both
animals
and
humans.
A
brief
summary
of
the
most
important
aspects
of
sodium
toxicokinetics
is
presented
below.

4.1
Absorption
Virtually
all
(­
99%)
of
the
sodium
ion
ingested
in
food
and
water
is
rapidly
absorbed
from
the
gastrointestinal
tract
(
Stipanuk
2000).
Sodium
crosses
the
brush
border
epithelial
membrane
of
the
intestine
through
sodium
channels
or
by
carried­
mediated
diffusion
down
an
electrochemical
gradient.
During
facilitated
transport,
sodium
can
carry
chloride
ion,
glucose,
amino
acids,
and
other
nutrients
into
the
intestinal
epithelial
cells.
Once
sodium
is
in
the
cytosol
of
the
brush
border
epithelial
cell,
it
is
actively
transported
into
the
blood
by
the
Na+/
K+­
ATPase
pump
located
in
the
basal
and
lateral
membrane
of
the
epithelial
cell
(
Stipanuk
2000).

4.2
Distribution
Once
absorbed,
the
sodium
ion
is
rapidly
distributed
throughout
the
body.
The
concentration
of
sodium
in
blood
and
other
extracellular
fluids
is
about
145
mM
(
3,335
mg/
L),
whereas
the
concentration
of
sodium
ion
inside
cells
is
about
12
mM
(
276
mg/
L)
(
Stipanuk
2000).
This
unequal
distribution
of
sodium
between
extracellular
and
intracellular
compartments
is
essential
to
the
normal
functioning
of
all
cells
and
tissues
of
the
body.

4.3
Metabolism
Sodium
ion
is
not
reactive
and
does
not
undergo
any
metabolic
reactions
in
the
traditional
sense
(
i.
e.,
it
is
not
transformed
by
enzymic
or
nonenzymic
mechanisms
into
any
altered
forms).
Sodium
does
function
as
a
counterion
for
macromolecules
such
as
DNA,
RNAs,
proteins,
and
sulfated
polysaccharides
that
carry
a
net
negative
change,
and
thus,
concentrations
can
be
enriched
in
the
microenviorinment
surrounding
macroion
surfaces
(
Stipanuk
2000).

4.4
Excretion
Sodium
is
excreted
mainly
in
the
urine,
although
some
sodium
loss
occurs
with
fecal
matter
and
in
perspiration.
The
kidney,
nervous
system,
and
endocrine
system
maintain
very
precise
control
of
renal
sodium
excretion,
with
approximately
95%
to
98%
of
the
sodium
being
reabsorbed
in
the
kidney
(
Stipanuk
2000).
In
the
proximal
tubule
of
the
kidney,
sodium
resorption
is
coupled
with
organic
solutes
and
anions
and
protons.
Entry
into
the
proximal
tubule
epithelium
is
mediated
by
symporter
(
e.
g.,
Na+­
glucose,
Na+­
PO
4
­
3,
Na+­
lactate,
and
Na+­
amino
acid
symporters)
and
antiporter
(
Na+­
H+
antiporter)
proteins
located
on
the
apical
membrane
of
the
proximal
tubule.
When
sodium
enters
the
cytoplasm
of
the
proximal
tubule,
it
is
actively
transported
into
the
blood
by
the
Na+/
K+­
ATPase
pump.
Similar
sodium
resorption
mechanisms
occur
in
the
loop
of
Henle
and
distal
tubule.

In
response
to
blood
volume
depletion
(
i.
e.,
decreased
blood
pressure),
the
sympathetic
nervous
system
stimulates
sodium
resorption.
Hormonal
control
of
sodium
resorption
is
dependent
on
renal
blood
flow
and
nervous
system
stimulation.
Decreased
renal
pressure
in
the
renal
arterioles,
as
well
as
sympathetic
nervous
system
stimulation,
results
in
the
kidney's
production
9
Sodium
 
February
2003
of
renin.
Renin
cleaves
circulating
angiotensinogen
to
form
angiotensin
I,
which
is
converted
to
angiotensin
II
by
angiotensin­
converting
enzyme
(
ACE),
an
enzyme
that
is
widely
distributed
in
the
body.
Angiotensin
II
stimulates
the
adrenal
gland
to
synthesize
aldosterone,
which
binds
to
receptors
in
the
cytoplasm
of
principal
cells
located
in
the
collecting
tubules
of
the
kidney,
and
stimulates
activity
of
the
apical
sodium
channel
and
basal
Na+/
K+­
ATPase
pump.
In
response
to
increased
blood
and
renal
pressure,
sympathetic
nervous
system
stimulation
and
aldosterone
synthesis
decrease
and
sodium
excretion
increases.
Of
the
approximately
25,200
mEq
of
sodium
filtered
through
the
kidneys
each
day,
150
mEq
is
excreted
(
Berne
and
Levy
1993,
Stipanuk
2000).

5.0
HEALTH
EFFECTS
DATA
5.1
Humans
Sodium
is
an
essential
nutrient
and
is
needed
to
maintain
body
fluid
volume
and
blood
pressure.
The
estimated
minimum
daily
requirement
for
healthy
adults
and
children
10
years
and
older
is
500
mg/
day
(
NRC
1989a).
At
birth,
the
estimated
minimum
requirement
ranges
from
100
to
200
mg/
day
and
increases
to
225
mg/
day
at
1
year
of
age.
The
minimum
requirement
increases
throughout
childhood
to
400
mg/
day
at
9
years
of
age.
Pregnancy
and
lactation
increase
the
minimum
requirement
by
69
and
135
mg/
day,
respectively
(
NRC
1989a).
No
optimal
level
of
sodium
intake
has
been
established
(
NRC
1989a).
The
kidneys
have
considerable
flexibility
in
removing
excess
sodium
and
can
accommodate
intakes
greater
than
the
minimum
requirements.

Because
sodium
is
a
common
constituent
of
food
and
water,
diseases
of
sodium
deficiency
in
humans
are
very
rare.
However,
excess
sodium
intake
can
cause
acute
and
long­
term
health
effects,
as
described
in
the
following
sections.
The
Dietary
Guidelines
for
Americans
(
USDA
2000)
recommend
2.4
g/
day
as
an
achievable
and
reasonable
goal
that
will
minimize
the
risk
for
sodium­
linked
hypertension
and
one
that
is
supported
by
other
recommendations
on
dietary
sodium
intake
(
AHA
2000,
NIH
1993,
NRC
1989a).

5.1.1
Short­
Term
Exposure
Studies
In
general,
sodium
salts
are
not
acutely
toxic
because
of
the
efficiency
with
which
mature
kidneys
excrete
sodium.
However,
acute
toxicity
and
death
have
been
reported
in
cases
of
very
high
sodium
intake.

Adults
Acute
effects
and
death
have
been
reported
in
cases
of
accidental
overdoses
of
sodium
chloride
(
WHO
1979).
Acute
effects
may
include
dryness
of
mucous
membranes,
violent
inflammatory
reaction
and
ulceration
in
the
gastrointestinal
tract,
along
with
dehydration
and
congestion
of
internal
organs,
particularly
the
meninges
and
brain.
Central
nervous
system
disturbances
such
as
convulsions,
confusion,
and
coma
may
result,
and
generalized
and
pulmonary
edema
are
possible.
Death
may
occur
from
respiratory
failure
secondary
to
an
acute
encephalopathy
(
MSDS
2000).
Two
cases
are
reported
by
WHO
(
1979)
of
individuals
who
sought
medical
10
Sodium
 
February
2003
attention
because
of
symptoms
experienced
after
using
drinking
water
sources
containing
greater
than
3
g
Na/
L.

Children
Infants
and
children
are
somewhat
more
susceptible
than
adults
to
the
effects
of
acute
overdoses
of
sodium
chloride
because
the
kidneys
of
immature
individuals
are
not
as
effective
in
controlling
sodium
levels
as
the
kidneys
of
adults
(
Sax
1975).
The
accidental
administration
of
infant
formula
containing
high
sodium
chloride
concentrations
(
dose
not
reported)
resulted
in
the
deaths
of
6
of
14
infants
(
Elton
et
al.
1963).
Kidney
lesions,
characterized
by
the
shrinkage
of
tubular
complexes
in
the
convoluted
kidney
tubules,
and
brain
thromboses
were
noted
at
autopsy.
Gauthier
et
al.
(
1969)
found
that
four
of
five
newborn
infants
who
received
sodium
at
concentrations
of
2,000
to
2,500
mEq/
L
(
46,000
 
57,500
mg/
L)
instead
of
sugar
in
formula
developed
hypernatremia
(
high
blood
sodium
concentrations)
and
died.
In
one
reported
case
(
DeGenaro
and
Nyhan
1971),
a
2­
year­
old
boy
died
9
days
after
being
given
a
dose
of
about
9,200
mg
Na/
kg
as
sodium
chloride
to
induce
vomiting.
Death
occurred
despite
medical
intervention.
The
child
was
hospitalized
within
2
hours
of
being
given
the
salt
solution.
He
was
in
a
coma.
His
temperature
was
elevated,
his
breathing
rapid
and
heartbeat
slow;
he
was
cyanotic
and
suffering
from
seizures.

5.1.2
Long­
Term
Exposure
Studies
Adults
A
large
body
of
evidence
suggests
that
excessive
sodium
intake
contributes
to
age­
related
increases
in
blood
pressure
and
may
contribute
to
essential
hypertension
(
AHA
2000,
NIH
1993,
NRC
1989a,
USDA
2000).
Estimates
based
on
the
1988
 
1991
National
Health
and
Nutrition
Examination
Survey
(
NHANES
III)
indicate
that
approximately
50
million
adults
have
high
blood
pressure
(
i.
e.,
systolic
pressure
$
140
mm
Hg
or
diastolic
pressure
$
90
mm
Hg),
with
the
prevalence
of
high
blood
pressure
increasing
with
age
(
NIH
1993).
High
blood
pressure
is
associated
with
an
increased
risk
of
developing
coronary
heart
disease,
stroke,
congestive
heart
failure,
renal
insufficiency,
and
peripheral
vascular
diseases.
However,
it
must
be
understood
that
high
blood
pressure
is
a
multifactorial
disorder,
with
dietary
sodium
as
one
of
a
number
of
factors
influencing
its
incidence.

The
Intersalt
Cooperative
Research
Group
(
ICRG)
performed
a
study
(
generally
referred
to
as
the
Intersalt
study)
that
suggests
blood
pressure
rises
with
increasing
sodium
consumption
(
ICRG
1988,
Elliott
et
al.
1989).
The
Intersalt
study
was
a
cross­
sectional
study
of
the
relationship
between
urinary
sodium
excretion
(
as
a
measure
of
sodium
intake)
and
blood
pressure,
involving
10,079
subjects
from
52
population
centers
in
32
countries.
The
study
included
approximately
equal
numbers
of
men
and
women
ages
20
to
59
years.
Estimated
regression
coefficients
of
blood
pressure
change
and
24­
hour
sodium
excretion,
calculated
after
adjusting
for
possible
confounders
such
as
age,
sex,
body
mass
index,
alcohol
consumption,
and
potassium
excretion,
indicated
an
increase
in
systolic
pressure
of
2.2
mm
Hg
for
every
100
mmol
(
2,300
mg)
increase
in
sodium
intake.
The
authors
indicated
that
the
positive
relationship
between
blood
pressure
and
sodium
intake
may
have
been
underestimated
because
some
of
the
subjects
included
in
the
11
Sodium
 
February
2003
study
were
(
1)
following
public
health
campaigns
against
a
high
salt
intake,
(
2)
taking
antihypertensive
medications,
or
(
3)
collecting
inadequate
urine
samples
for
sodium
intake
measurements
(
Elliott
et
al.
1989).

Stamler
(
1991)
evaluated
the
impacts
of
changes
in
sodium
intake
on
mortality
due
to
coronary
artery
disease,
stroke,
and
other
diseases.
The
author
estimated
that
a
nationwide
reduction
of
2.2
mm
Hg
in
average
systolic
blood
pressure
would
result
in
a
4%
reduction
in
coronary
disease
mortality,
a
6%
reduction
in
stroke
mortality,
and
a
3%
overall
reduction
in
other
deaths.
This
drop
in
total
mortality
would
result
in
12,000
fewer
deaths
each
year
in
Americans
aged
45
to
64.
Decreases
in
sodium
intake
from
average
levels
to
100
mmol/
day
(
2,300
mg/
day)
throughout
the
lifespan
would
correspond
to
a
reduction
of
9
mm
Hg
in
the
expected
increase
in
systolic
blood
pressure
from
age
25
to
55.
This
would
translate
into
a
mortality
rate
reduction
of
16%
for
coronary
heart
disease,
23%
for
stroke,
and
13%
for
death
from
all
causes.
The
author
concluded
that
sodium
remains
the
key
risk
factor
for
essential
hypertension
when
compared
with
other
risk
factors
such
as
body
mass
index
and
alcohol
consumption.

Frost
et
al.
(
1991)
performed
a
meta­
analysis
of
14
published
studies
from
the
United
States,
Europe,
and
Asia
that
measured
blood
pressure
and
sodium
intake
estimated
by
24­
hour
urinary
sodium
excretion
in
12,773
subjects.
The
analysis
indicated
that
there
is
a
highly
significant
(
p<
0.001)
positive
association
between
blood
pressure
and
sodium
intake
within
populations.
Elliott
(
1991)
performed
a
similar
meta­
analysis
of
14
observational
studies
in
16
populations
relating
24­
hour
urinary
sodium
excretion
and
blood
pressures.
This
analysis
also
indicated
positive
and
significant
correlations
with
both
systolic
and
diastolic
blood
pressure
in
males
and
females.
For
men
and
women
combined
(
12,503
subjects),
the
regression
coefficient
(
corrected
for
reliability)
indicated
systolic
and
diastolic
blood
pressures
were
lowered
by
about
3.7
and
2.0
mm
Hg,
respectively,
per
100
mmol
(
2,300
mg)
reduction
in
24­
hour
urinary
sodium
excretion
(
p<
0.001).
This
analysis
did
not
include
Intersalt
data.

Sullivan
(
1991)
analyzed
data
on
183
subjects
to
determine
sodium
sensitivity
(
increase
of
mean
blood
pressure
of
more
than
5%
when
progressing
from
low­
to
high­
sodium
intake).
Using
this
criterion,
sodium
sensitivity
was
detected
in
15%
of
white
normotensive
subjects,
29%
of
white
borderline
hypertensive
subjects,
27%
of
normotensive
black
subjects,
and
50%
of
black
borderline
hypertensive
subjects.
Long­
term
followup
of
sodium­
sensitive
and
sodium­
resistant
individuals
with
similar
blood
pressures
indicated
that
a
daily
sodium
intake
of
about
150
mEq
(
3,450
mg)
resulted
in
significantly
higher
blood
pressure
and
forearm
vascular
resistance
in
the
sodium­
sensitive
group.
Sodium
intake
may
also
influence
the
heart
muscle
thickness
as
a
secondary
response
to
blood
pressure
effect.
Dietary
salt
intake,
as
determined
by
24­
hour
urinary
sodium
excretion,
was
significantly
correlated
(
p<
0.001)
to
left
ventricular
hypertrophy
(
wall
thickness)
in
a
series
of
42
hypertensive
individuals
(
Schmieder
et
al.
1988).

A
randomized
clinical
trial
of
2,382
men
and
women
(
30
to
54
years
of
age)
with
high
normal
blood
pressure
(
diastolic
83
to
89
mm
Hg
and
systolic
below
140
mm
Hg)
and
elevated
body
weight
(
110%
to
165%
of
the
recommended
value)
was
conducted
at
nine
academic
medical
centers
over
a
3­
year
period
(
Trials
of
Hypertension
Prevention
Collaborative
Research
Group
1997).
Subjects
were
divided
into
four
groups.
One
group
was
treated
for
weight
reduction,
the
second
for
reduced
sodium
intake
(
1.8
g/
day
or
less),
and
the
third
for
combined
weight
12
Sodium
 
February
2003
reduction
and
reduced
sodium
intake.
The
last
group
received
usual
care
and
served
as
the
control.
Both
weight
loss
and
sodium
restriction
alone
or
in
combination
were
associated
with
a
decrease
in
blood
pressure
at
the
end
of
6
months
and
at
3
years.
Weight
loss
alone
had
a
greater
impact
on
blood
pressure
when
compared
to
the
usual
control
group
than
did
sodium
restriction
at
six
months
(
3.7/
2.7
mm
Hg
vs.
2.9/
1.6
mm
hg).
The
greatest
reduction
in
blood
pressure
was
observed
in
the
group
that
combined
weight
loss
with
sodium
restriction
(
4.0/
2.8
mm
Hg).
After
3
years,
the
treatment
groups
still
had
lower
blood
pressures
than
the
usual
care
group,
but
the
reductions
in
blood
pressure
were
rather
comparable
in
the
weight
reduction
(
1.3/
0.9
mm
Hg),
sodium
restriction
(
1.2/
0.7
mm
Hg),
and
combination
groups
(
1.1/
0.6
mm
Hg).
The
authors
felt
that
this
was
a
reflection
of
the
difficulties
involved
with
long­
term
behavior
modification
to
sustain
weight
loss
and
low­
sodium
intakes.

Numerous
investigations
have
analyzed
the
reduction
in
blood
pressure
following
a
reduction
in
sodium
intake,
both
in
hypertensive
and
normotensive
individuals.
A
meta­
analysis
of
56
trials
(
28
with
1,131
hypertensive
subjects
and
28
with
2,374
normotensive
subjects)
found
a
significant
reduction
in
systolic
blood
pressure
of
3.7
mm
Hg
(
p<
0.001)
in
the
hypertensives
and
1.0
mm
Hg
(
p<
0.001)
for
normotensives
for
a
100
mmol
per
day
(
2,300
mg/
day)
reduction
in
daily
sodium
excretion
(
Midgley
et
al.
1996).
These
findings
were
supported
by
other
studies
(
Graudal
et
al.
1998,
Cutler
et
al.
1991).
However,
other
clinical
studies
have
not
detected
convincing
evidence
of
a
protective
effect
of
low
sodium
intake
on
the
risk
of
cardiovascular
disease
(
Muntzel
and
Drueke
1992,
Salt
Institute
2000,
NIH
1993,
Callaway
1994,
Kotchen
and
McCarron
1998,
McCarron
1998).
Even
though
the
experts
at
the
National
Heart,
Lung
and
Blood
Institute
support
the
policy
of
universal
salt
reduction
for
decreasing
the
risk
for
essential
hypertension,
the
scientific
experts
at
the
AHA,
American
Society
of
Hypertension,
and
the
European
and
International
Societies
of
Hypertension
disagree
with
the
universal
salt
reduction
hypothesis
(
Taubes
1998).

Dietary
studies
are
difficult
to
analyze
because
changing
the
concentration
of
one
nutrient
in
the
diet
changes
the
balance
of
all
the
other
nutrients
as
well.
It
becomes
difficult
to
determine
if
the
observed
effect
is
the
result
of
the
decrease
in
the
target
nutrient
or
the
change
in
the
balance
of
all
nutrients.
In
the
mid­
1990s,
the
National
Heart,
Lung
and
Blood
Institute
sponsored
a
study
of
hypertension
and
diet
called
the
Dietary
Approaches
to
Stop
Hypertension
(
DASH)
trial.
The
subjects
were
459
adults
classified
as
hypertensives
who
did
not
use
antihypertensive
medications
during
the
trial.
The
subjects
were
divided
into
three
groups
that
received
either
the
control
diet,
a
diet
high
in
fruits
and
vegetables,
or
a
combination
diet
that
was
still
rich
in
fruits
and
vegetables
but
had
higher
amounts
of
low­
fat
animal
protein
and
grains
than
the
high
fruit
and
vegetable
diet
(
Vogt
et
al.
1999).
The
subjects
consumed
their
respective
diets
as
prepared
by
the
study
kitchen
for
an
8­
week
period.
The
sodium
content
of
all
three
diets
was
the
same
(
3
g/
day)
and
greater
than
the
present
dietary
guideline
for
sodium
(
2.4
g/
day).
The
high
fruit
and
vegetable
and
combination
diets
were
2
to
3
times
higher
in
potassium,
calcium,
magnesium,
and
fiber
than
the
control
diet.
The
combination
diet
reduced
average
blood
pressures
by
5.5
mm
Hg
(
systolic)
and
3
mm
Hg
(
diastolic)
compared
with
the
control
diet.
The
high
fruit
and
vegetable
diet
reduced
blood
pressures
by
2.8
mm
Hg
(
systolic)
and
1.1
mm
Hg
(
diastolic)
compared
with
the
control
diet.
These
reductions
are
similar
to
those
obtained
in
many
of
the
sodium
restriction
diets.
13
Sodium
 
February
2003
In
a
followup
to
the
original
DASH
study,
the
effects
of
different
levels
of
dietary
sodium
in
conjunction
with
the
combination
DASH
diet
were
evaluated
(
Sacks
et
al.
2001,
Svetkey
et
al.
1999).
All
subjects
had
higher
than
optimal
blood
pressure.
Systolic
blood
pressures
exceeded
120
mm
Hg
but
were
not
higher
than
159
mm
Hg
(
the
cutoff
for
stage
1
hypertension).
Diastolic
blood
pressures
were
higher
than
80
mm
Hg,
but
not
higher
than
95
mmHg.
After
an
initial
adjustment
period
on
a
high­
sodium
(
150
mmol/
day)
control
diet,
the
412
subjects
were
randomly
assigned
to
either
the
combination
DASH
diet
or
a
control
diet.
Diets
for
both
groups
had
three
sodium
levels
(
low,
50
mmol/
day;
intermediate,
100
mmol/
day;
or
high,
150
mmol/
day),
which
were
administered
for
30
consecutive
days
in
random
order
in
a
crossover
design.
Meals
were
supplied
to
the
participants
for
the
duration
of
the
study.

For
those
in
the
control
group,
reducing
sodium
intake
from
the
high
to
the
intermediate
level
lowered
systolic
blood
pressure
by
2.1
mm
Hg;
reducing
sodium
intake
from
the
intermediate
to
the
low
level
lowered
systolic
blood
pressure
by
an
additional
4.6
mm
Hg
(
Sacks
et
al.
2001).
Subjects
on
the
DASH
diet
had
a
1.3
and
1.7
mm
Hg
reduction
in
systolic
blood
pressure
when
sodium
intake
was
reduced
from
high
to
intermediate
level
and
intermediate
to
low
level,
respectively.
At
the
high,
intermediate,
and
low
sodium
intake
levels,
systolic
blood
pressure
was
reduced
by
5.9,
5.0,
and
2.2
mm
Hg,
respectively,
in
subjects
on
the
DASH
diet
compared
with
subjects
on
the
control
diet.
The
effect
on
systolic
blood
pressure
was
greater
in
hypertensive
subjects
(
systolic
140
S
159
mm
Hg;
diastolic
90
S
95
mm
Hg)
compared
with
nominal
normotensives
(
systolic
120
S
140
mm
Hg;
diastolic
80
S
90
mm
Hg).
The
average
reduction
in
blood
pressure
achieved
from
sodium
restriction
was
greater
for
those
on
the
control
diet
than
for
those
on
the
DASH
diet,
for
African­
Americans
on
the
control
diet
than
for
other
participants,
and
for
women
on
the
DASH
diet
than
for
men
on
the
DASH
diet.

Decreases
in
diastolic
blood
pressure
were
correlated
with
reduction
in
sodium
levels
in
both
the
DASH
and
control
diets.
Diastolic
pressure
was
lower
at
all
sodium
levels
in
subjects
on
the
DASH
diet
compared
with
subjects
on
the
control
diet.
The
magnitude
of
reduction
in
diastolic
blood
pressure
was
not
as
great
as
that
reported
for
systolic
blood
pressure.
The
study
authors
concluded
that
reducing
sodium
intake
to
below
the
current
recommendation
of
100
mmol/
day
and
the
DASH
diet
both
lower
blood
pressure
substantially,
with
a
greater
reduction
in
blood
pressure
occurring
when
the
low
sodium
and
DASH
diet
are
combined.
They
acknowledged
the
limitation
of
the
30­
day
experimental
period.
Compliance
with
the
low­
salt
dietary
plan
might
decrease
with
time
because
a
large
portion
of
the
sodium
in
the
American
diet
comes
from
processed
foods
rather
than
from
home
use
of
table
salt.

One
study
suggests
that
low
sodium
intake
may
actually
increase
the
risk
for
cardiovascular
disease
in
adults.
Alderman
et
al.
(
1995)
reported
the
relationship
between
morbidity
and
mortality
due
to
cardiovascular
disease
in
hypertensive
subjects
and
their
urinary
sodium
excretion.
The
study
cohort
included
2,937
hypertensive
subjects
(
1,900
men
and
1,037
women).
The
principal
finding
was
that
low
urinary
sodium
excretion
was
associated
with
high
incidences
of
heart
attacks
in
hypertensive
men
and
hypertensive
subjects
(
men
and
women
combined),
but
not
in
hypertensive
women.
In
men,
age­
and
race­
adjusted
myocardial
infarction
incidence
was
11.5
versus
2.5
in
the
lowest
versus
highest
urinary
sodium
excretion
groups.
The
hypertensive
subjects
with
high
sodium
intakes
did
not
experience
high
incidences
of
myocardial
infarction
when
compared
with
subjects
on
normal
sodium
diets.
A
group
of
scientific
experts
who
14
Sodium
 
February
2003
commented
on
this
study
concluded
that
future
research
may
be
needed
to
clarify
this
observation,
as
the
study
was
not
a
randomized
trial
and
did
not
address
possible
confounders
such
as
smoking
and
alcohol
use
(
AHA
1995).

Children
A
number
of
studies
have
investigated
the
relationship
between
sodium
intake
from
water
and
blood
pressure
in
children.
Most
of
these
studies
have
not
detected
an
association
between
sodium
in
drinking
water
(
at
concentrations
ranging
from
5
to
583
mg/
L)
and
increased
blood
pressure
in
children
(
Pomrehn
et
al.
1983,
Faust
1982,
Armstrong
et
al.
1982,
Tuthill
et
al.
1980,
Colditz
and
Willett
1985),
although
a
few
studies
do
suggest
an
increase
in
blood
pressure
with
the
high
sodium
intake
(
Calabrese
and
Tuthill
1977,
1981,
Tuthill
and
Calabrese
1979,
Fatula
1967).

Summary
Excessive
intake
of
very
high
doses
of
sodium
(
accidental
poisoning)
may
cause
acute
effects
such
as
nausea,
vomiting,
inflammatory
reaction
in
the
gastrointestinal
tract,
thirst,
muscular
twitching,
convulsions,
and
possibly
death.
For
long­
term
lower
level
exposures,
the
health
effect
of
primary
concern
is
essential
hypertension.
Although
evidence
of
a
positive
association
between
sodium
intake
and
blood
pressure
and
essential
hypertension
is
convincing,
numerous
studies
fail
to
find
a
protective
effect
of
low
sodium
intake
in
controlling
blood
pressure
in
hypertensive
subjects.
Because
of
the
inconsistencies
and
uncertainties
in
the
data
on
the
relationship
between
sodium
intake
and
cardiovascular
disease,
it
is
not
possible
to
draw
definite
conclusions
on
the
benefits
of
reduced
sodium
intake.
Factors
such
as
increased
intake
of
potassium,
calcium,
and
magnesium,
reduced
caloric
intake,
reduced
chloride
intake,
moderate
physical
activity,
and
lower
alcohol
consumption
may
play
a
significant
role
in
reducing
blood
pressure
and
the
risk
for
cardiovascular
disease.
Sodium
restriction
seems
to
be
the
most
beneficial
in
lowering
blood
pressure
for
older
persons
who
are
only
mildly
hypertensive
and
are
not
overweight.

5.1.3
Sensitive
Populations
Several
studies
have
shown
that
children
are
more
sensitive
than
adults
to
high
sodium
intake
(
Elton
et
al.
1963,
Gauthier
et
al.
1969,
DeGenaro
and
Nyhan
1971).
This
increased
sensitivity
is
associated
with
the
lower
ability
of
the
immature
kidney
to
control
sodium
levels
compared
with
that
of
the
adult
kidney.
However,
on
a
mg/
kg
basis,
the
sodium
requirement
for
infants
and
children
is
greater
than
that
for
adults
(
NRC
1989a).

In
addition
to
children,
the
elderly
may
be
more
sensitive
to
adverse
health
effects
resulting
from
high
sodium
exposure.
This
is
because
the
elderly
have
a
higher
incidence
of
cardiovascular
disease
(
including
high
blood
pressure)
than
do
younger
subjects
(
Sowers
and
Lester
2000).
Therefore,
the
hypertensive
effects
of
sodium
may
be
more
severe
in
the
elderly.
In
addition,
because
the
elderly
tend
to
have
a
higher
taste
threshold
for
salt
(
Hyde
and
Feller
1981,
Stevens
1996),
they
may
have
a
higher
salt
intake.
African­
Americans
are
more
susceptible
to
sodium­
15
Sodium
 
February
2003
induced
adverse
health
effects
because
of
high
prevalence
of
hypertension
and
increased
salt
sensitivity
among
this
population
(
Sullivan
1991,
Svetkey
et
al.
1996,
1999).

Individuals
with
decreased
renal
function
or
renal
insufficiency
are
more
sensitive
to
high
sodium
intake
than
are
individuals
with
healthy
kidneys.
Sodium
chloride
at
200
mmol/
day
significantly
elevated
systolic
blood
pressure
in
humans
with
chronic
renal
failure
(
Muntzel
and
Drueke
1992).
In
addition,
renal
tubule
defects
or
alterations
in
kidney
hemodynamics
have
been
postulated
to
predispose
salt­
sensitive
individuals
to
retain
sodium.
Sodium
retention
has
been
reported
in
rats
given
high
doses
of
sodium
chloride
following
partial
nephrectomy.
Dietary
sodium
restrictions
are
recommended
for
individuals
with
acute
or
chronic
renal
problems
and
those
with
nephritic
syndrome
(
Whitney
et
al.
1987).
Renal
problems
are
associated
with
about
10%
of
the
hypertension
in
the
population.

5.2
Animal
Studies
5.2.1
Short­
Term
Exposure
Studies
Sodium
ion
(
ingested
as
sodium
chloride)
has
low
acute
toxicity
in
animals.
Doses
that
cause
lethality
in
animals
range
from
around
3,000
to
8,000
mg/
kg
(
HSDB
2000,
RTECS
2002).
Death
has
been
attributed
to
severe
alterations
in
fluid
concentrations
and/
or
fluid
volumes
(
HSDB
2000).

5.2.2
Long­
Term
Exposure
Studies
Hypertension
has
been
clearly
demonstrated
in
several
species
of
animals
given
high
concentrations
of
sodium
chloride
in
their
diets
(
WHO
1979).
Dahl
(
1967)
exposed
21­
day­
old
female
Sprague­
Dawley
rats
to
a
diet
containing
8%
sodium
chloride
for
12
to
15
months.
This
corresponds
to
a
dose
of
about
1,570
mg/
kg
sodium
ion,
based
on
EPA's
reference
values
of
340
g/
bw
and
a
food
intake
of
17
g/
day
(
assuming
a
rat
consumes
5%
of
its
body
weight
per
day)
(
U.
S.
EPA
1988).
Within
6
to
9
months,
about
75%
of
the
rats
exhibited
hypertension,
and
their
mean
blood
pressure
increased
with
age.
Rats
maintained
on
the
low­
salt
diet
(
0.35%
sodium
chloride,
corresponding
to
a
dose
of
70
mg/
kg
sodium
ion)
did
not
exhibit
a
corresponding
increase
in
blood
pressure
with
age.

5.2.3
Reproductive
Studies
High
doses
of
sodium
chloride
(
1,570
mg
sodium/
kg
body
weight)
have
been
observed
to
cause
reproductive
effects
in
various
strains
of
pregnant
rats.
Effects
on
the
dams
have
included
decreases
in
pregnancy
rates
and
maternal
body
weight
gain.

The
reproductive
effects
of
sodium
ion
were
studied
in
three
strains
of
pregnant
rats
(
SHR,
WKY,
and
Sprague­
Dawley)
ranging
in
age
from
3
months
to
1
year
(
Karr­
Dullien
and
Bloomquist
1979).
It
should
be
noted
that
SHR
rats
are
bred
to
be
hypertensive
and
serve
as
a
hypertensive
rat
model.
The
animals
were
fed
diets
containing
either
0.4
or
8.0%
sodium
chloride
(
corresponding
to
doses
of
79
or
1,570
mg/
kg
sodium
ion,
based
on
EPA's
reference
values
of
340
g
bw
and
17
g/
food/
day)
throughout
gestation
and
lactation
(
U.
S.
EPA
1988).
16
Sodium
 
February
2003
Pregnancy
rates
were
decreased
by
38%
in
SHR
rats
and
by
66%
in
WKY
rats
in
the
high­
salt
diet
groups
compared
with
those
in
the
low­
salt
diet
groups.
The
high­
salt
diet
also
decreased
the
maternal
body
weight
gain
in
SHR
and
WKY
rats.
This
effect
was
also
noted
in
SHR
rats
fed
with
low­
salt
diets.
No
effects
were
observed
in
Sprague­
Dawley
rats.

5.2.4
Developmental
Studies
In
a
continuation
to
the
above­
mentioned
study,
the
pups
from
the
low­
and
high­
dose
dams
were
placed
on
either
a
0.4%
or
8%
sodium
chloride
diet
irrespective
of
the
dams'
diets
(
Karr­
Dullien
and
Bloomquist
1979).
This
dosing
regimen
resulted
in
four
dose
groups:
high­
dose
pups
from
high­
dose
dams
(
HH),
high­
dose
pups
from
low­
dose
dams
(
HL),
low­
dose
pups
from
high­
dose
dams
(
LH),
and
low­
dose
pups
from
low­
dose
dams
(
LL).
After
11.5
weeks
of
exposure,
significant
increases
in
systolic
blood
pressure
were
noted
in
SHR
HH
pups
compared
with
all
other
pups.
This
was
accompanied
by
a
63%
mortality
rate
after
4
months
of
exposure
due
to
peripheral
capillary
hemorrhage
and
stroke.
No
significant
changes
in
blood
pressure
or
mortality
were
observed
in
the
WKY
or
Sprague­
Dawley
pups.

No
developmental
effects
were
observed
in
the
offspring
of
mice
administered
189
mg/
kg
sodium
ion
or
rats
administered
147
mg/
kg
sodium
ion
on
days
6
S
15
of
gestation
(
Fregly
1981).

5.2.5
Genotoxicity
Studies
Sodium
(
as
sodium
chloride)
produced
DNA
damage
in
mammalian
assays
employing
mouse
lymphocytes
(
2.3
g/
L),
induced
unscheduled
DNA
synthesis
in
rats
(
16.8
g/
kg),
and
caused
DNA
damage
in
hamster
ovaries
(
6.3
g/
L)
(
RTECS
2002).
Tests
in
Saccharomyces
cerevisia
(
46
g/
L)
and
Escherichia
coli
(
3.5
g/
L)
were
also
positive.
However,
the
overall
importance
of
these
findings
is
questionable
because
these
studies
used
very
high
sodium
levels
that
would
tend
to
disrupt
the
cellular
osmotic
balance
and
DNA
microenvironment,
especially
in
the
in
vitro
studies.

5.2.6
Cancer
Studies
Sodium
by
itself
is
not
believed
to
cause
cancer.
However,
several
studies
suggest
that
sodium
chloride
may
enhance
the
cancer
risk
caused
by
other
chemicals
(
NRC
1989b).
For
example,
the
incidences
of
gastric
tumors
caused
by
4­
nitroquinoline­
1­
oxide
and
N­
methyl­
N1­
nitro­
Nnitrosoguanidine
were
reported
to
be
enhanced
by
simultaneous
sodium
chloride
administration
(
10%
of
diet
or
in
their
drinking
water)
to
male
Wistar
rats
(
Tatematsu
et
al.
1975).
The
authors
hypothesized
that
the
promoting
effect
of
the
concentrated
sodium
chloride
was
a
consequence
of
its
ability
to
disrupt
the
mucopolysaccharide
layer
lining
the
gastric
epithelium.

This
indirect
effect
of
sodium
in
enhancing
cancer
risk
might
be
due
to
cell
death
in
the
gastrointestinal
tract
and
resulting
cell
regeneration
(
as
measured
by
ornithine
decarboxylase
activity
and
DNA
synthesis).
For
example,
a
single
oral
dose
of
a
saturated
sodium
chloride
solution
resulted
in
a
200­
fold
increase
in
ornithine
decarboxylase
activity
within
6
hours
and
a
ninefold
increase
in
DNA
synthesis
within
3
hours
in
rat
stomach
mucosa
(
Furihata
et
al.
1984).
Subsequent
studies
indicated
that
sources
of
sodium
other
than
sodium
chloride
may
also
cause
17
Sodium
 
February
2003
damage
to
the
gastrointestinal
tract
(
Furihata
et
al.
1989).
These
sources
included
the
sodium
salts
of
acetic,
L­
ascorbic,
L­
glutamic,
carbonic,
and
sorbic
acid.

6.0
ORGANOLEPTIC
PROPERTIES
Organoleptic
properties
for
contaminants
in
drinking
water
refer
to
odor,
color,
and
taste.
Because
these
characteristics
do
not
cause
adverse
health
effects,
they
are
not
used
by
EPA
for
developing
primary
water
standards.
However,
organoleptic
properties
are
used
in
establishing
secondary
standards
and
guidelines.

Several
studies
are
available
that
report
on
the
organoleptic
properties
of
sodium
in
drinking
water;
they
focused
primarily
on
taste
threshold
of
sodium
chloride
in
drinking
water.
None
of
the
studies
reported
odor
thresholds
for
sodium
salts
or
distinguished
between
threshold
levels
and
levels
that
are
unpalatable.

The
taste
threshold
concentration
of
sodium
in
drinking
water
depends
on
the
associated
anion.
For
example,
Schiffman
et
al.
(
1980)
reported
considerable
differences
in
the
overall
taste
sensation
of
tested
salts
due
to
the
associated
anions.
Taste
threshold
was
tested
in
12
students
(
6
males
and
6
females,
18
 
25
years)
using
several
sodium
salts
dissolved
in
deionized
water
(
0.2
M
Na+;
4.6
g
Na+/
L).
The
salts
that
were
perceived
to
be
the
most
"
salty"
were
sodium
chloride
and
sodium
bromide,
whereas
sodium
citrate
was
perceived
to
be
the
least
salty.
The
taste
threshold
of
sodium
chloride
was
dependent
on
whether
sodium
chloride
was
in
mixture
with
other
chemicals
(
e.
g.,
sucrose
and/
or
citric
acid).
Stevens
and
Traverzo
(
1997)
reported
that
the
taste
threshold
for
sodium
chloride
increases
three
to
four
times
in
a
mixture
with
sucrose
or
citric
acid,
and
more
than
nine
times
in
a
mixture
with
sucrose
and
citric
acid
compared
with
sodium
chloride
in
water.

Age
may
also
affect
the
taste
threshold.
Stevens
(
1996)
reported
that
the
salt
threshold
is
much
lower
in
younger
subjects
(
18
 
29
years,
n=
15)
than
in
older
subjects
(
66
 
90
years,
n=
15).
Subjects
were
offered
5
mL
of
distilled
water
or
the
salt
solution
and
asked
to
choose
the
one
with
the
salty
taste.
The
mean
taste
threshold
values
for
sodium
chloride
(
as
sodium)
dissolved
in
deionized
water
for
younger
and
older
subjects
were
1.3
mM
(
30
mg
Na+/
L)
and
5.7
mM
(
131
mg
Na+/
L),
respectively.
The
average
response
for
both
groups
was
2.7
mM
(
60
mg/
L).
Work
by
Pangborn
and
Pecore
(
1982)
discussed
below
suggests
that
the
fact
that
the
participants
knew
they
were
to
identify
a
salty
taste
influenced
the
results
of
this
study.

Pangborn
and
Pecore
(
1982)
reported
the
taste
threshold
of
sodium
among
44
females
and
13
males
(
18
 
22
years
old)
who
were
stratified
as
having
high
(
n=
14),
medium
(
n=
26),
or
low
dietary
intakes
of
salt
(
n=
17),
based
on
food
habit.
Solutions
of
0.005%­
0.12%
sodium
chloride
(
20
S
472
mg
Na+/
L)
in
double­
distilled
water
were
tested.
The
study
design
was
similar
to
that
used
by
Stevens
(
1996),
except
that
the
directions
given
to
the
subjects
varied.
In
one
test,
the
subjects
were
asked
to
choose
the
container
that
had
a
taste
and
then
to
identify
the
taste.
The
mean
detection
thresholds
reported
for
the
sodium
chloride
in
water
ranged
from
0.015
to
0.031%
(
60
to
122
mg
Na+/
L)
and
the
selection
of
the
container
with
the
salt
was
correct
for
77%
to
85%
of
the
trials.
The
mean
taste
thresholds
for
the
individual
groups
are
given
in
Table
6­
1.
18
Sodium
 
February
2003
Table
6­
1.
Mean
Taste
Threshold
Values
in
Young
Adults
with
Different
Sodium
Intake
Levels
Sodium
Chloride
Intake
Groupa
Number
of
Subjects
Mean
Taste
Threshold
Valuesb
Mean
Taste
Threshold
Valuesc
Low
17
122
mg
Na+/
L
40
mg
Na+/
L
Medium
26
87
mg
Na+/
L
48
mg
Na+/
L
High
14
60
mg
Na+/
L
32
mg
Na+/
L
a
Denotes
the
arbitrary
assessment
of
dietary
sodium
intake
through
questionnaires.
Excerpted
from
Pangborn
and
Pecore
(
1982).
b
When
subjects
were
not
told
that
the
taste
to
be
recognized
was
salt.
c
When
subjects
were
told
that
the
taste
to
be
recognized
was
salt.

Despite
the
fact
that
the
subjects
could
correctly
identify
the
container
with
the
salt,
they
did
not
initially
recognize
that
taste
as
salty.
For
the
same
group
of
subjects,
the
concentration
that
could
be
identified
as
having
a
salty
taste
was
2.5
to
almost
4
times
higher
than
the
concentration
that
could
be
tasted.
In
addition,
participants
were
able
to
correctly
identify
the
taste
as
salty
only
35%
to
49%
of
the
time.
These
results
suggest
that
taste
recognition
was
greater
for
the
high­
salt
intake
group
than
for
the
other
groups
and
that
the
ability
to
taste
salt
and
the
ability
to
correctly
identify
the
taste
are
different.

In
a
second
portion
of
their
study,
Pangborn
and
Pecore
(
1982)
used
the
same
study
design
but
told
the
subjects
to
select
between
distilled
water
and
a
solution
that
contained
salt.
Under
these
conditions,
the
ability
to
make
a
correct
selection
increased
to
more
than
90%
and
the
average
taste
threshold
dropped
to
a
level
comparable
to
that
recorded
by
Stevens
(
1996).
The
threshold
for
the
high­
salt
group
was
32
mg/
L
and
those
for
the
low
and
medium
groups
were
40
and
48
mg/
L,
respectively.
A
hypothesis
for
the
high
salt­
taste
sensitivity
in
the
high­
intake
group
was
not
provided.
Their
high
salt
intake
had
apparently
not
acclimatized
them
to
the
salt
taste.

Weiffenbach
et
al.
(
1982)
reported
the
mean
taste
threshold
values
for
sodium
chloride
in
deionized
water
as
2.49
mM
(
57
mg
Na+/
L),
3.26
mM
(
75
mg
Na+/
L),
and
6.1
mM
(
140
mg
Na+/
L)
for
subjects
#
45
years,
46
 
65
years,
and
>
65
years,
respectively.
The
low
end
of
the
threshold
in
this
data
set
is
comparable
to
that
in
the
Pangborn
and
Pecore
(
1982)
study.
The
study
designs
were
very
similar
and
it
appears
that,
like
Pangborn
and
Pecore
(
1982),
Weiffenbach
et
al.
(
1982)
did
not
reveal
the
nature
of
the
tastant
to
the
participants.
Somewhat
higher
taste
threshold
values
were
reported
by
Hyde
and
Feller
(
1981)
for
younger
adults.
The
taste
threshold
for
sodium
chloride
dissolved
in
deionized
water
in
young
adults
(
mean
age
28
years,
n=
24)
and
elderly
persons
(
mean
age
75
years,
n=
24)
was
10
mM
(
230
mg
Na+/
L)
and
20
mM
(
460
mg
Na+/
L),
respectively.

According
to
WHO
(
1993),
the
average
taste
threshold
for
sodium
(
as
sodium
chloride)
at
room
temperature
is
about
200
mg/
L,
a
value
that
was
used
as
the
WHO
drinking
water
guideline.
However,
as
illustrated
by
the
data
discussed
above,
the
taste
threshold
may
vary
substantially
among
individuals
and
as
a
function
of
other
solutes
that
may
be
present
in
the
water.
For
example,
Stevens
(
1996)
combined
salt
with
sugar
(
sweet),
citric
acid
(
sour),
or
quinine
19
Sodium
 
February
2003
hydrochloride
(
bitter)
in
a
series
of
binary
mixtures
and
demonstrated
that
one
tastant
influences
the
ability
to
detect
the
second
tastant
in
a
mixture.

It
is
not
possible
to
identify
point
threshold
values
for
the
taste
of
sodium
in
drinking
water,
because
the
concentration
will
vary
among
individuals,
for
the
same
individual
at
different
times,
and
for
different
water
matrices,
water
temperatures,
and
many
other
variables
(
e.
g.,
age,
masking
due
to
other
tastants,
and
the
anion
forming
the
salt).
However,
the
data
discussed
above
suggest
that
30
to
60
mg/
L
is
a
threshold
for
the
ability
to
taste,
but
not
necessarily
to
identify,
the
presence
of
sodium
chloride
in
water.

7.0
CHARACTERIZATION
OF
HAZARD
AND
DOSE­
RESPONSE
7.1
Hazard
Characterization
Sodium
is
a
physiologically
important
element
needed
to
maintain
normal
body
fluid
volume
and
blood
pressure
and
normal
cell
function.
The
normal
sodium
level
in
the
blood
is
154
mM
(
3,542
mg/
L).
Intake
from
food
is
generally
the
major
source
of
sodium,
with
only
a
small
contribution
from
drinking
water.

The
NRC
estimated
minimum
daily
requirements
for
sodium
are
120
 
225
mg
for
infants
(
0
months
S
1
year),
300
S
400
mg
for
children
(
2
 
9
years),
and
500
mg
for
individuals
10
years
old
and
older.
Requirements
increase
during
pregnancy
and
lactation.
Minimum
requirements
are
easily
supplied
by
the
average
American
diet.
The
AHA
and
NAS
recommend
that
for
healthy
adults
2,400
mg/
day
is
a
prudent,
achievable
dietary
intake
for
sodium
that
will
help
lower
the
risk
for
hypertension
in
sodium­
sensitive
individuals
(
AHA
2000,
NIH
1993,
NRC
1989a,
USDA
2000).
Average
daily
intakes
are
closer
to
3,500
to
4,500
mg/
day
(
Karanja
et
al.
1999).

About
3%
of
the
population
is
on
sodium­
restricted
diets,
which
sometimes
require
sodium
intakes
of
less
than
500
mg
(~
1/
4
teaspoon)
per
day.
Sodium­
restricted
diets
limit
sodium
exposure
to
levels
of
250,
500,
1,000,
or
2,000
mg/
day.
Each
of
these
diets
achieves
sodium
restriction
by
limiting
the
types
and
amounts
of
specific
foods
that
can
be
eaten.
A
no­
added­
salt
diet
restricts
only
those
foods
that
are
high
in
sodium
(
e.
g.,
bacon
and
potato
chips).
The
sodium
content
of
such
a
diet
averages
about
4,000
mg/
day
(
Cataldo
and
Whitney
1986).
The
fact
that
such
a
diet
exceeds
the
dietary
goal
for
sodium
intake
is
indicative
of
the
degree
to
which
sodium
is
present
in
the
food
supply.
Individuals
on
sodium­
restricted
diets
are
advised
to
find
out
and
consider
the
amount
of
sodium
in
their
drinking
water
supply
when
planning
their
diet.

In
general,
sodium
salts
are
not
acutely
toxic
to
humans,
and
sodium
salts
generally
have
low
acute
toxicity
in
animals
(
HSDB2000).
However,
acute
effects
and
death
have
been
reported
in
cases
of
very
high
sodium
intake
(
WHO
1979).
The
effects
due
to
ingestion
of
high
sodium
concentrations
tend
to
be
more
severe
for
infants
than
adults
because
of
the
immaturity
of
infant
kidneys
(
Sax
1975).

Hypertension
due
to
high
sodium
intake
was
originally
demonstrated
in
sodium­
sensitive
SHR
rats
(
Dahl
1967).
Numerous
studies
conducted
in
humans
suggest
that
excessive
sodium
intake
contributes
to
age­
related
increases
in
blood
pressure,
leading
to
hypertension
in
sensitive
20
Sodium
 
February
2003
individuals
(
WHO
1979,
NIH
1993).
The
Intersalt
study
suggested
that
blood
pressure
rises
with
increasing
sodium
consumption.
This
study,
which
included
10,079
subjects
from
52
population
centers
in
32
countries,
reported
an
increase
in
systolic
pressure
of
2.2
mm
Hg
for
every
100
mmol
(
2,300
mg)
increase
in
sodium
intake
(
ICRG
1988,
Elliott
et
al.
1989).
A
positive
relationship
between
sodium
intake
and
blood
pressure
is
also
indicated
by
other
investigators
(
Frost
et
al.
1991,
Elliott
1991).
Increases
in
blood
pressure
are
associated
with
increases
in
mortality
due
to
coronary
artery
disease
and
stroke
(
Stamler
1991).
Sodium
intake
may
also
result
in
an
increase
in
heart
muscle
thickness
as
a
secondary
response
to
increased
blood
pressure
(
Schmieder
et
al.
1988).

Reports
on
blood
pressure
and
sodium
intake
in
children
are
inconsistent.
Several
researchers
have
failed
to
find
an
association
between
sodium
concentrations
in
the
drinking
water
and
increased
blood
pressure
in
children
(
Pomrehn
et
al.
1983,
Faust
1982,
Armstrong
et
al.
1982,
Tuthill
et
al.
1980,
Colditz
and
Willett
1985),
whereas
other
studies
suggest
an
increase
in
blood
pressure
with
a
high
sodium
intake
(
Calabrese
and
Tuthill
1977,
1981,
Tuthill
and
Calabrese
1979).

Several
clinical
trials
examining
the
beneficial
effect
of
decreased
sodium
intake
did
not
yield
convincing
evidence
of
a
protective
effect
of
low
sodium
intake
on
reducing
the
risk
of
cardiovascular
disease
in
normotensive
populations
(
Muntzel
and
Drueke
1992,
Salt
Institute
2000,
NIH
1993,
Callaway
1994,
Kotchen
and
McCarron
1998,
McCarron
1998).
However,
the
recent
results
of
the
DASH
and
DASH
II
trials
suggest
that
dietary
changes
with
sodium
restriction
are
beneficial
for
many
with
hypertension
(
Harsha
et
al.
1999,
Sacks
et
al.
2001).
Heart­
healthy
diets
involve
weight
reduction,
exercise,
stress
reduction,
and
adequate
dietary
intake
of
potassium,
calcium,
and
magnesium
as
well
as
restriction
of
sodium
(
Whitney
et
al.
1987).
Evidence
suggests
that
chloride
restriction
also
favors
lowered
blood
pressure
(
Boegehold
and
Kotchen
1991,
Shore
et
al.
1988).
However,
because
most
of
the
added
sodium
in
prepared
foods
is
sodium
chloride,
decreased
chloride
intake
usually
accompanies
decreased
sodium
intake.
Limiting
cholesterol,
dietary
fat,
and
alcohol
intake
are
also
recommended
(
Whitney
et
al.
1987).
Older
individuals
with
mild
essential
hypertension
and
average
body
weights
seem
to
have
the
most
successful
response
to
dietary
salt
restriction
(
Stipanuk
2000).

Data
on
the
reproductive
toxicity
of
sodium
are
sparse.
High
doses
of
sodium
chloride
(
1,570
mg
sodium/
kg
body
weight)
have
been
reported
to
cause
maternal
effects
in
rats.
The
maternal
toxicity
included
decreased
pregnancy
rates
and
maternal
body
weight
gain.
Developmental
effects
included
increased
blood
pressure
and
high
mortality
(
Karr­
Dullien
and
Bloomquist
1979).
However,
these
developmental
effects
were
observed
only
in
SHR
rat
pups
(
a
type
of
rat
specifically
bred
to
be
hypertensive)
fed
high­
sodium
diets
for
up
to
4
months
after
parturition.
This
study
also
reported
no
developmental
effects
in
Sprague­
Dawley
or
WKY
rat
pups
(
both
normotensive
strains
of
rat).

There
is
no
evidence
that
sodium
is
a
carcinogen
and
it
does
not
appear
to
be
genotoxic.
High
oral
doses
of
sodium
chloride
may
increase
the
incidence
of
gastric
tumors
in
the
presence
of
other
carcinogens
through
mechanisms
such
as
damage
to
the
gastrointestinal
tract
followed
by
increased
DNA
synthesis
and
cell
regeneration
(
Tatematsu
et
al.
1975,
NRC
1989b,
Takahashi
et
al.
1983).
21
Sodium
 
February
2003
Populations
that
are
expected
to
have
an
increased
sensitivity
to
sodium
include
individuals
with
hypertension,
the
elderly
(
blood
pressure
increases
with
age),
African­
Americans
(
the
incidence
of
salt­
sensitivity
and
hypertension
is
disproportionately
high
among
African­
Americans),
and
individuals
with
renal
problems.

7.2
Characterization
of
Organoleptic
Effects
Studies
on
the
organoleptic
properties
of
sodium
in
drinking
water
focus
primarily
on
the
taste
threshold
of
sodium
chloride.
The
taste
threshold
for
sodium
chloride
is
dependent
on
whether
sodium
chloride
is
in
a
mixture
with
other
compounds
(
e.
g.,
sucrose
and/
or
citric
acid),
the
age
of
the
subjects,
and
on
whether
or
not
the
target
taste
is
identified
beforehand
(
Weiffenbach
et
al.
1982,
Stevens
1996,
Hyde
and
Feller
1981,
Pangborn
and
Pecore
1982).

Several
studies
suggest
that
taste
threshold
varies
between
younger
and
older
subjects
(
Stevens
1996,
Weiffenbach
et
al.
1982,
Hyde
and
Feller
1981).
The
taste
threshold
for
sodium
chloride
dissolved
in
deionized
water
in
young
adults
(
mean
age
28
years,
n=
24)
and
elderly
persons
(
mean
age
75
years,
n=
24)
was
230
and
460
mg
Na+/
L,
respectively
(
Hyde
and
Feller
1981).
Stevens
(
1996)
reported
that
lower
taste
threshold
values
were
observed
in
younger
subjects
(
18
 
29
years,
n=
15)
compared
with
older
subjects
(
66
 
90
years,
n=
15).
The
mean
taste
threshold
values
for
sodium
chloride
dissolved
in
deionized
water
for
younger
and
older
subjects
were
30
and
131
mg
Na+/
L,
respectively.

The
mean
taste
thresholds
for
sodium
chloride
in
water
for
normotensive
young
adults
ranged
from
60
to
122
mg
Na+/
L
when
the
target
taste
was
not
identified
and
from
32
to
48
mg/
L
when
the
target
taste
was
identified
(
Pangborn
and
Pecore
1982).
Weiffenbach
et
al.
(
1982)
reported
a
mean
taste
threshold
of
57
mg
Na+/
L.
In
the
1982
study
by
Pangborn
and
Pecore,
individuals
who
habitually
have
a
high­
salt
diet
had
a
lower
taste
threshold
than
those
who
habitually
consumed
less
salt.

Because
the
threshold
value
for
the
taste
of
sodium
in
drinking
water
varies
as
a
function
of
dietary
habit,
age,
temperature,
masking
by
other
tastants,
the
anion
associated
with
sodium,
and
other
factors,
no
single
value
can
be
identified
as
a
unique
threshold
value.
The
studies
by
Pangborn
and
Pecore
(
1982)
and
Weiffenbach
et
al.
(
1982)
indicate
a
mean
taste
threshold
of
approximately
60
mg/
L
when
the
nature
of
the
taste
was
not
identified.
When
the
nature
of
the
taste
was
identified,
the
average
threshold
for
young
adults
was
approximately
30
mg/
L
(
Pangborn
and
Pecore
1982,
Stevens
1996).
On
the
basis
of
these
values,
30
to
60
mg/
L
is
the
lower
end
of
the
taste
threshold,
and
many
individuals
will
not
be
able
to
detect
the
presence
of
sodium
in
drinking
water
except
at
higher
concentrations.

7.3
Dose­
Response
Characterization
Although
numerous
human
studies
have
examined
sodium
intake
and
blood
pressure
effects,
these
studies
are
not
adequate
to
serve
as
key
studies
for
dose­
response
characterization
for
the
following
reasons:
(
1)
the
dose­
response
relationships
varied
among
the
different
studies,
(
2)
sodium
intake
measurements
were
generally
indirect
(
determined
by
the
amount
of
sodium
excreted
in
the
urine),
and
(
3)
the
results
may
have
been
influenced
by
other
nutrients
in
diet,
22
Sodium
 
February
2003
lifestyle,
and
behavior
in
addition
to
sodium
(
Muntzel
and
Drueke
1992,
Salt
Institute
2000,
NIH
1993,
Callaway
1994,
Kotchen
and
McCarron
1998,
McCarron
1998).

The
data
on
dose­
response
are
fraught
with
controversy.
The
AHA
(
2000),
NIH
(
1993),
and
NRC
(
1989a)
recommend
that
healthy
adults
restrict
their
sodium
intake
to
no
more
than
2,400
mg/
day.
Lowering
sodium
intake
by
100
mmol/
day
(
2,300
mg/
day)
from
average
levels
(­
3,500
S
4,500
mg/
day)
lowers
systolic
blood
pressure
for
sodium­
sensitive
individuals
by
3.7
mmHg
compared
with
1
mm
Hg
in
normotensive
individuals.
However,
dietary
changes
that
increased
calcium,
potassium,
magnesium,
and
fiber
but
did
not
change
sodium
(
DASH
diet)
were
able
to
achieve
similar
reductions
in
systolic
pressure
in
a
hypertensive
population
(
Harsha
et
al.
1999).
A
combination
of
the
DASH
diet
with
sodium
restriction
achieved
additional
reductions
in
blood
pressure
among
hypertensive
and
normotensive
subjects
(
Sacks
et
al.
2001).
However,
accomplishing
a
reduction
in
population
exposure
to
sodium
presents
a
challenge
because
most
of
the
sodium
comes
from
processed
foods
rather
than
from
discretionary
use
of
table
salt.
Sacks
et
al.
(
2001)
in
their
presentation
of
the
DASH­
sodium
results
encouraged
incentives
that
would
commercially
increase
the
availability
of
low­
salt
products.

Data
from
NIRS
and
SDWA
monitoring
of
sodium
levels
in
PWSs
have
shown
that
the
median
levels
of
sodium
detected
are
generally
below
30
mg/
L.
However,
many
PWSs
reported
sodium
levels
greater
than
120
mg/
L,
and
the
99th
percentile
of
the
samples
in
NIRS
was
517
mg/
L.
For
persons
on
sodium­
restricted
diets,
sodium
concentrations
greater
than
120
mg/
L
could
be
problematic
(
i.
e.,
could
cause
an
increase
in
blood
pressure)
if
sodium
levels
in
water
remained
elevated
for
a
significant
period
of
time.

This
Drinking
Water
Advisory
recommends
that
the
sodium
concentration
in
drinking
water
not
exceed
a
range
of
30
to
60
mg/
L
because
of
possible
adverse
effects
on
taste
at
higher
concentrations.
Concentrations
below
30
mg/
L
contribute
less
than
1.5%
of
the
sodium
in
an
average
American
diet
and
less
than
2.5%
of
the
present
sodium
guideline
value,
assuming
consumption
of
2
L
of
tap
water
per
day.
For
a
concentration
of
60
mg/
L,
the
comparable
values
are
3%
and
5%.

EPA
requires
Public
Water
Systems
that
exceed
20
mg/
L
to
notify
local
and
State
public
health
officials(
U.
S.
EPA
1996).
The
EPA
guidance
was
developed
for
those
individuals
restricted
to
a
total
sodium
intake
of
500
mg/
day
(
U.
S.
EPA
1976)
and
should
not
be
extrapolated
to
the
entire
population.

EPA
requires
periodic
monitoring
of
sodium
at
the
entry
point
to
the
distribution
system.
Monitoring
is
to
be
conducted
annually
for
surface
water
systems
and
every
3
years
for
groundwater
systems
(
40CFR:
141.41,
US
EPA
1996).
The
water
supplier
must
report
sodium
test
results
to
local
and
State
public
health
officials
by
direct
mail
within
3
months
of
the
analysis,
unless
this
responsibility
is
assumed
by
the
State.
This
provides
the
public
health
community
with
information
on
sodium
levels
in
drinking
water.
23
Sodium
 
February
2003
8.0
REFERENCES
Abraham
S,
Carroll
MD.
1981.
Fats,
cholesterol
and
sodium
intake
in
the
diet
of
persons
1
 
74
years:
United
States.
Advance
Data
No.
54.
Washington,
DC:
U.
S.
Department
of
Health,
Education
and
Welfare
(
as
cited
in
NRC
1989a).

American
Heart
Association
(
AHA).
Sodium.
2000.
AHA
Recommendation.
http://
www.
americanheart.
org/
Heart_
and
_
Stroke_
A_
Z_
Guide/
sodium.
html.

AHA.
1995.
Study
suggests
a
link
between
low
urinary
salt
levels
and
higher
risk
of
heart
attack
in
hypertensive
men.
AHA
Health
and
Science
News.
NR
95­
4286­(
Hypert/
Alderman).

Alderman
MH,
Madhavan
S,
Cohen
H,
Sealey
JE,
Laragh
JH.
1995.
Low
urinary
sodium
is
associated
with
greater
risk
of
myocardial
infarction
among
treated
hypertensive
men.
Hypertension
25:
1144
 
1152.

Armstrong
BK,
Margetts
BM,
McCall
MG,
Binns
CW,
Campbell
NA,
Masarei
JRL.
1982.
Water
sodium
and
blood
pressure
in
rural
school
children.
Arch
Environ
Health
37:
236
 
245.

Berne
RM,
Levy
MN.
1993.
Physiology,
3rd
ed.
Mosby­
Year
Book,
Inc.

Boegehold
MA,
Kotchen
TA.
1991.
Importance
of
dietary
chloride
for
salt
sensitivity
of
blood
pressure.
Hypertention
17
(
Suppl1):
1­
158
to1­
161.

Budavari
S.
1996.
Merck
Index,
12th
ed.
Merck
&
Co.

Cadmus.
2001.
Sodium:
Occurrence
and
Exposure
S
Support
for
Candidate
Contaminant
List
(
CCL)
Public
Notification
of
Draft
Regulatory
Determinations.
Submitted
to
the
U.
S.
Environmental
Protection
Agency,
Office
of
Water.
Contract
No.
68­
C­
99­
206.

Calabrese
EJ,
Tuthill
RW.
1981.
The
influence
of
elevated
levels
of
sodium
in
drinking
water
on
elementary
and
high
school
students
in
Massachusetts.
Sci
Total
Environ
18:
117
 
133.

Calabrese
EJ,
Tuthill
RW.
1977.
Elevated
blood
pressure
and
high
sodium
levels
in
the
public
drinking
water.
Arch
Environ
Health
35:
200.

Callaway
W.
1994.
Re­
examining
cholesterol
and
sodium
recommendations.
Nutrition
Today
29:
32
 
36.

Cataldo
CB,
Whitney
EN.
1986.
Nutrition
and
Diet
Therapy:
Principles
and
Practice.
St.
Paul,
MN:
West
Publishing
Co.
http://
www.
ccohs.
ca/
ccohs.
html.

Chemistry
Explorer.
2000.
Sodium.
http://
www.
iversonsoftware.
com/
reference/
chemistry/
sodium.
htm.
24
Sodium
 
February
2003
Clayton
GD,
Clayton
FE.
1981.
Patty's
industrial
hygiene
and
toxicology.
Vol.
2.
New
York:
John
Wiley
and
Sons,
pp.
2056
 
2057.

Colditz
GA,
Willett
WC.
1985.
Epidemiological
methods
employed
in
the
study
of
the
influence
of
elevated
drinking
water
sodium
on
blood
pressure:
a
critique
in:
Proceedings
of
Conference
on
Inorganics
in
Drinking
Water
and
Cardiovascular
Disease.
In:
Calabrese
et
al.
eds.
Amherst,
MA,
p.
99.

Cutler
JA,
Follmann
D,
Elliott
P,
Suh
I.
1991.
An
overview
of
randomized
trials
of
sodium
reduction
and
blood
pressure.
Hypertension
17(
Suppl
I):
I­
27
 
I­
33.

Dahl
LK.
1967.
Effects
of
chronic
excess
salt
ingestion
S
experimental
hypertension
in
the
rat:
correlation
with
human
hypertension.
In:
Elliot
GB,
Alexander
EA,
eds.
Sodium
from
drinking
water
as
an
unsuspected
cause
of
cardiac
decompensation.
Circulation
23:
562
 
566.

DeGenaro
F,
Nyhan
WL.
1971.
Salt
 
a
dangerous
"
antidote."
J
Pediatr
78:
1048
 
1049.

Elliott
P.
1991.
Session
I:
epidemiological
overview.
Observational
studies
of
salt
and
blood
pressure.
Hypertension
17(
Suppl
I):
I­
3
 
I­
8.

Elliott
P,
Marmot
M,
Dyer
A,
Joossens
J,
Kesteloot
H,
Stamler
R,
Stamler
J,
Rose
G.
1989.
The
intersalt
study.
Main
results,
conclusions
and
some
implications.
Clin
Exper
Hyper­
Theory
and
Practice
A11:
1025
 
1034.

Elton
NW,
Elton
WJ,
Narzareno
JP.
1963.
Pathology
of
acute
salt
poisoning
in
infants.
Am
J
Clin
Pathol
39:
252
 
264.

Fairbridge
RW.
1972.
Cyclic
Salts.
In:
Fairbridge
RW,
ed.
The
Encyclopedia
of
Geochemistry
and
Environmental
Sciences.
New
York:
Van
Nostrand
Reinhold,
p.
216.

Fatula
MI.
1967.
The
frequency
of
arterial
hypertension
among
persons
using
water
with
an
elevated
sodium
chloride
content.
Sov
Med
30:
123.

Faust
HS.
1982.
Effects
of
drinking
water
and
total
sodium
intake
on
blood
pressure.
Am
J
Clin
Nutr
35:
1459
 
1467.

Fregly
MJ.
1981.
Sodium
and
potassium.
Ann
Rev
Nutr
1:
69
 
93.

Frost
CD,
Law
MR,
Wald
NJ.
1991.
By
how
much
does
dietary
salt
reduction
lower
blood
pressure?
II.
Analysis
of
observational
data
within
populations.
BMJ
302:
815
 
818.

Furihata
C,
Sato
Y,
Hosaka
M,
Matsushima
T,
Furukawa
F,
Takahashi
M.
1984.
NaCl
induced
ornithine
decarboxylase
and
DNA
synthesis
in
rat
stomach
mucosa.
Biochem
Biophys
Res
Commun
121:
1027
 
1032.
25
Sodium
 
February
2003
Furihata
C,
Yamakoshi
A,
Takezawa
R,
Matsushima
T.
1989.
Various
sodium
salts,
potassium
salts,
a
calcium
salt
and
an
ammonium
salt
induced
ornithine
decarboxylase
and
stimulated
DNA
synthesis
in
rat
stomach
mucosa.
Jpn
J
Cancer
Res.
80:
424
 
429.

Gauthier
B,
Freeman
R,
Beveridge
J.
1969.
Accidental
salt
poisoning
in
hospital
nursery.
Aust
Pediat
J
5:
101
 
105.

Graudal
NA,
Galloe
AM,
Garred
P.
1998.
Effects
of
sodium
restriction
on
blood
pressure,
renin,
aldosterone,
catecholamines,
cholesterols,
and
triglyceride.
A
meta­
analysis.
JAMA
279:
1383
 
1391.

Harsha
DW,
Pao­
Hwa
L,
Obarzanek
E,
Karanja
NM,
Moore
TJ,
Caballero
B.
1999.
Dietary
approaches
to
stop
hypertension:
A
summary
of
results.
J
Am
Diet
Assoc
99(
8):
S35
 
S39.

Hyde
RJ,
Feller
RP.
1981.
Age
and
sex
effects
on
taste
of
sucrose,
NaCl,
citric
acid
and
caffeine.
Neurobiol
Aging
2:
315
 
318.

HSDB.
2000.
Hazardous
Substances
Data
Bank.
National
Library
of
Medicine,
Bethesda,
MD.
March
23,
2000.

Intersalt
Cooperative
Research
Group
(
ICRG).
1988.
Intersalt:
An
international
study
of
electrolyte
excretion
and
blood
pressure:
results
for
24­
hour
urinary
sodium
and
potassium
excretion.
BMJ
297:
319
 
328.

Karanja
NM,
Obarzanek
E,
Pao­
Hwa
L,
McCullough
ML,
Phillips
KM,
Swain
JF,
Champagne
CM,
Hoben
KP.
1999.
Descriptive
characteristics
of
the
dietary
patterns
used
in
the
Dietary
Approaches
to
Stop
Hypertension
trial.
J
Am
Diet
Assoc
99(
8):
S19
 
S27.

Karr­
Dullien
V,
Bloomquist
E.
1979.
The
influence
of
prenatal
salt
on
the
development
of
hypertension
by
spontaneously
hypertensive
rats
(
SHR)
(
40462).
Proc
Soc
Exp
Biol
Med
160:
421
 
425.

Kostick
DS.
1993.
The
material
flow
of
salt.
Information
Circular
9343.
Washington,
DC:
U.
S.
Department
of
the
Interior,
Bureau
of
Mines,
p.
31.

Kotchen
TA,
McCarron
DA.
1998.
Dietary
electrolytes
and
blood
pressure.
A
statement
for
healthcare
professionals
from
the
American
Heart
Association
Nutrition
Committee.
Circulation
98:
613
 
617.

Kurtzweil
P.
1995.
Scouting
for
sodium
and
other
nutrients
important
to
blood
pressure.
Washington,
DC:
U.
S.
Food
and
Drug
Administration,
FDA
Consumer.
http://
www.
americanheart.
org/
Heart_
and
_
Stroke_
A_
Z_
Guide/
sodium.
html.
July
21,
2000.

McCarron
DA.
1998.
Diet
and
blood
pressure
 
The
paradigm
shift.
Science
281:
933
 
934.
26
Sodium
 
February
2003
Mickelson
O,
Makdani
D,
Gill
JL,
Frank
RL.
1977.
Sodium
and
potassium
intakes
and
excretions
of
normal
men
consuming
sodium
chloride
or
a
1:
1
mixture
of
sodium
and
potassium
chloride.
Am
J
Clin
Nutr
30:
2033
(
as
cited
in
NRC
1989a).

Midgley
JP,
Matthew
AG,
Greenwood
CMT,
Logan
AG.
1996.
Effect
of
reduced
dietary
sodium
on
blood
pressure.
A
meta­
analysis
of
randomized
controlled
trials.
JAMA
275:
1590
 
1597.

MSDS.
2000.
Material
safety
data
sheet
for
sodium
chloride
from
University
of
California
MSDS
database.
March
27,
2000.
http://
mc2.
cchem.
berkeley.
edu/
Chem10/
chloride.
html.

Muntzel
M,
Drueke
T.
1992.
A
comprehensive
review
of
the
salt
and
blood
pressure
relationship.
Am
J
Hypertension
5:
1S
 
42S.

National
Academy
of
Sciences
(
NAS).
1977.
Drinking
water
and
health.
Washington,
DC:
National
Academy
Press,
pp.
400
 
411.

National
Institutes
of
Health
(
NIH).
1993.
Working
group
report
on
primary
prevention
of
hypertension.
NIH
Publication
No.
93­
2669.

National
Research
Council
(
NRC).
1989a.
Recommended
dietary
allowances.
Washington,
DC:
National
Academy
of
Sciences,
National
Academy
Press,
pp.
247
 
261.

NRC.
1989b.
Committee
on
Diet
and
Health
Food
Nutrition
Board,
Commission
on
Life
Sciences.
Diet
and
health:
implications
for
reducing
chronic
disease
risk.
Washington,
DC:
National
Academy
Press,
pp.
413
 
430.

National
Science
Foundation
International
(
NSF).
1997.
Drinking
water
treatment
chemicals
S
health
effects.
American
National
Standards/
NSF
International
Standard.
Ann
Arbor,
MI.

Pangborn
RM,
Pecore
SD.
1982.
Taste
perception
of
sodium
chloride
in
relation
to
dietary
intake
of
salt.
Am
J
Clin
Nutr
35:
510
 
520.

Pennington
JAT,
Wilson
DB,
Newell
RF,
Harland
BF,
Johnson
RD,
Vanderveen
JE.
1984.
Selected
minerals
in
food
surveys,
1974
to
1981/
82.
J
Am
Diet
Assoc
84:
771
 
780
(
as
cited
in
NRC
1989a).

Pomrehn
PR,
Clarke
WR,
Sowers
MF,
Wallace
RB,
Lauer
RM.
1983.
Community
differences
in
blood
pressure
levels
and
drinking
water
sodium.
Am
J
Epidemiol
118:
60
 
71.

Registry
of
Toxic
Effects
of
Chemical
Substances
(
RTECS).
2002.
Database.
Cincinnati,
OH:
National
Institute
for
Occupational
Safety
and
Health.
March
28,
2000.
uhttp://
www.
cdc.
gov/
niosh/
rtecs.
html.

Sacks
FM,
Svetkey
LP,
Vollmer
WM,
Appel
LJ,
Bray
GA,
Harsha
D,
Obarzanek
E,
Conlin
PR,
Miller
ER
III,
Simons­
Morton
DG,
Karanja
N,
Lin
PH.
2001.
Effects
on
blood
pressure
of
27
Sodium
 
February
2003
reduced
dietary
sodium
and
the
dietary
approaches
to
stop
hypertension
(
DASH)
diet.
N
Engl
J
Med
344(
1):
53
 
55.

Salt
Institute.
2000.
SI
Report.
March
6,
2000.
http://
www.
saltinstitute.
org/
news00­
8.
html.

Sanchez­
Castillo
CP,
Branch
WJ,
James
WP.
1987b.
A
test
of
the
validity
of
the
lithium­
marker
technique
for
monitoring
dietary
sources
of
salt
in
men.
Clin
Sci
72:
87
 
94
(
as
cited
in
NRC
1989a).

Sanchez­
Castillo
CP,
Warrender
S,
Whitehead
TP,
James
WP.
1987a.
An
assessment
of
the
sources
of
dietary
salt
in
a
British
population.
Clin
Sci
72:
95
 
102
(
as
cited
in
NRC
1989a).

Sax
NI.
1975.
Dangerous
properties
of
industrial
materials,
4th
ed.
New
York:
Van
Nostrand
Reinhold
Company,
p.
1101.

Sax
NI,
Lewis
RJ.
1987.
Hawley's
condensed
chemical
dictionary,
11th
ed.
New
York:
Van
Nostrand
Reinhold
Company,
pp.
1050
 
1051.

Schiffman
SS,
McElroy
AE,
Erickson
RP.
1980.
The
range
of
taste
quality
of
sodium
salts.
Physiol
Behav
24:
217
 
224.

Schmieder
RE,
Messerli
FH,
Garavaglia
GE,
Nunez
BD.
1988.
Dietary
salt
intake.
A
determinant
of
cardiac
involvement
in
essential
hypertension.
Circulation
78:
951
 
956.

Shacklette
HT,
Boerngen
JG.
1984.
Element
concentrations
in
soils
and
other
surficial
materials
of
the
conterminous
United
States.
U.
S.
Geological
Survey
Professional
Paper
1270.

Shore
AC,
Markandy
ND,
MacGregor
GA.
1986.
A
randomized
crossover
study
to
compare
the
blood
pressure
response
to
sodium
loading
with
and
without
chloride
in
patients
with
essential
hypertension.
J.
Hypertention
6:
616­
617.

Sittig
M.
1981.
Handbook
of
toxic
and
hazardous
chemicals
and
carcinogens,
2nd
ed.
Park
Ridge,
NJ:
Noyes
Publications,
pp.
792
 
793.

Sowers
JR,
Lester
M.
2000.
Hypertension,
hormones,
and
aging.
Lab
Clin
Med
135:
379
 
386.

Stamler
R.
1991.
Implications
of
the
Intersalt
study.
Hypertension
17(
Suppl
I):
I­
16
 
I­
20.

Stevens
JC.
1996.
Detection
of
tastes
in
mixture
with
other
tastes:
issues
of
masking
and
aging.
Chem
Senses
21:
211
 
221.

Stevens
JC,
Traverzo
A.
1997.
Detection
of
a
target
taste
in
a
complex
masker.
Chem
Senses
22:
529
 
534.

Stipanuk
MH.
2000.
Biochemical
and
Physiological
Aspects
of
Human
Nutrition.
Philadelphia:
WB
Saunders
Co,
pp.
686
 
710.
28
Sodium
 
February
2003
Subar
AF,
Krebs­
Smith
SM,
Cook
A,
Kahle
LL.
1998.
Dietary
sources
of
nutrients
among
U.
S.
adults,
1989
to
1991.
J
Am
Diet
Assoc
98(
5):
537
S
547.

Sullivan
JM.
1991.
Salt
sensitivity.
Definition,
conception,
methodology,
and
long­
term
issues.
Hypertension
17(
Suppl
I):
I
S
61
 
I
S
68.

Svetkey
LP,
Mckeown
SP,
Wilson
AF.
1996.
Heritability
of
salt
sensitivity
in
black
Americans.
Hypertension
28:
854
 
858.

Svetkey
LP,
Sacks
FM,
Obarzanek
E,
Vollmer
WM,
Appel
LJ,
Karanja
N,
Harsha
D,
Bray
GA,
Aickin
M,
Proschan
M,
Windhauser
MM,
Swain
JF,
McCarron
PB,
Rhodes
DG,
Laws
RL.
1999.
The
DASH
diet,
sodium
intake
and
blood
pressure
trial
(
DASH­
Sodium):
rationale
and
design.
J
Am
Diet
Assoc
99:
S96
 
S104.

Tatematsu
M,
Takahashi
M,
Fukushima
S,
Hananouchi
M,
Shirai
T.
1975.
Effects
in
rats
of
sodium
chloride
on
experimental
gastric
cancers
induced
by
N­
methyl­
N1­
nitro­
Nnitrosoguanidine
or
4­
nitroquinoline­
1­
oxide.
J
Nat
Cancer
Inst
55:
101
 
106.

Taubes
G.
1998.
The
(
political)
science
of
salt.
Science
281:
898
 
907.

Trials
of
Hypertension
Prevention
Collaborative
Research
Group.
1997.
Effects
of
weight
loss
and
sodium
reduction
intervention
on
blood
pressure
and
hypertension
incidence
in
overweight
people
with
high
normal
blood
pressure.
The
Trials
of
Hypertension
Prevention,
Phase
II.
Arch
Intern
Med
157:
657
 
667.

Tuthill
RW,
Calabrese
EJ.
1979.
Elevated
sodium
levels
in
the
public
drinking
water
as
a
contributor
to
elevated
blood
pressure
levels
in
the
community.
Arch
Environ
Health
37:
197
(
as
cited
in
U.
S.
EPA
1992).

Tuthill
RW,
Sonich
C,
Okun
A,
Greathouse
D.
1980.
The
influence
of
naturally
and
artificially
elevated
levels
of
sodium
in
drinking
water
on
blood
pressure
in
school
children.
J
Environ
Pathol
Toxicol
3:
173
 
181.

U.
S.
Department
of
Agriculture
(
USDA).
2000.
Nutrition
and
Your
Health:
Dietary
Guidelines
for
Americans,
5th
ed.
Home
and
Garden
Bulletin
No.
232.
U.
S.
Department
of
Health
and
Human
Services,
Washington,
DC.

U.
S.
Environmental
Protection
Agency
(
U.
S.
EPA).
1976.
National
Interim
Primary
Drinking
Water
Regulations.
Office
of
Water
Supply.
EPA­
570/
9­
76­
003.

U.
S.
EPA.
1988.
Recommendation
for
and
documentation
of
biological
values
for
use
in
risk
assessment.
Environmental
Criteria
and
Assessment
Office,
Office
of
Health
and
Environmental
Assessment,
Office
of
Research
and
Development,
Cincinnati,
OH.
EPA/
600/
6­
87/
008.
29
Sodium
 
February
2003
U.
S.
EPA.
1996.
Code
of
Federal
Regulations:
Protection
of
the
Environment.
Parts
126­
149.
Section
141.41.
Office
of
the
Federal
Register,
National
Archives
and
Records
Administration.
Washington
DC.
pp.
352­
353.

Vogt
TM,
Appel
LJ,
Obarzanek
E,
Moore
TJ,
Vollmer
WM,
Svetkey
LP,
Sacks
FM,
Bray
GA,
Cutler
JA,
Windhauser
MM,
Pao­
Hwa
L,
Karanja
NM.
1999.
Dietary
approaches
to
stop
hypertension:
rationale,
design,
and
methods.
J
Am
Diet
Assoc
99(
8):
S12
 
S18.

Weiffenbach
JM,
Baum
BJ,
Burghauser
R.
1982.
Taste
thresholds:
quality
specific
variation
with
human
aging.
J
Gerontol
37:
372
 
377.

Whitney
EN,
Cataldo
CB,
Rolfes
SR.
1987.
Understanding
Normal
and
Clinical
Nutrition.
St.
Paul,
MN:
West
Publishing
Co.

World
Health
Organization
(
WHO).
1979
Sodium,
chlorides
and
conductivity
in
drinking
water.
EURO
reports
and
studies.
No.
2.
Copenhagen,
Denmark:
WHO
Regional
Office
for
Europe.

WHO.
1993.
World
Health
Organization.
Guidelines
for
drinking­
water
quality,
2nd
ed.
Vol
1.
Recommendations.
Geneva,
Switzerland.