Document ID: EPA-HQ-OW-2003-0074-0276
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2003-12-24T05:00Z

National
Report
on
Human
Exposure
to
Environmental
Chemicals
March
24,
2003
The
National
Report
on
Human
Exposure
to
Environmental
Chemicals
provides
an
ongoing
assessment
of
the
U.
S.
population's
exposure
to
environmental
chemicals
using
biomonitoring.
This
information
is
collected
in
the
National
Health
and
Nutrition
Examination
Survey
(
NHANES)
conducted
by
CDC's
National
Center
for
Health
Statistics.
The
report
can
be
viewed
online
at
http://
www.
cdc.
gov/
exposurereport/
pdf/
SecondNER.
pdf.

Purpose:
The
overall
purpose
of
the
report
is
to
provide
unique
exposure
information
to
scientists,
health
officials
and
others
to
help
prevent
disease
that
results
from
exposure
to
environmental
chemicals.
Some
of
the
specific
public
health
uses
of
the
exposure
information
are:
°
To
determine
which
chemicals
get
into
Americans
and
at
what
concentrations
°
For
chemicals
with
a
known
toxicity
level,
to
determine
the
prevalence
of
people
with
levels
above
those
toxicity
levels
(
e.
g.
lead)
°
To
establish
reference
ranges
that
can
be
used
by
physicians
and
scientists
to
determine
whether
a
person
or
group
has
an
unusually
high
exposure
°
To
assess
the
effectiveness
of
public
health
efforts
to
reduce
exposure
of
Americans
to
specific
chemicals
°
To
determine
whether
exposure
levels
are
higher
among
minorities,
children,
women
of
childbearing
age,
or
other
potentially
vulnerable
groups
°
To
track,
over
time,
trends
in
levels
of
exposure
of
the
population
°
To
set
priorities
for
research
on
human
health
Chemicals:
The
first
report
presented
exposure
data
for
27
chemicals
from
NHANES
1999.
The
second
report
presents
biomonitoring
exposure
data
for
116
environmental
chemicals,
including
the
27
in
the
first
report.
The
first
report
measured
lead,
mercury,
cadmium,
and
other
metals;
dialkyl
phosphate
metabolites
of
organophosphate
pesticides;
cotinine;
and
phthalates.
The
second
report
includes
these
chemicals
and
adds:
°
Polycyclic
aromatic
hydrocarbons
(
PAHs)
°
Dioxins,
furans,
and
coplanar
polychlorinated
biphenyls
(
BCPs)
°
Non­
coplanar
PCBs
°
Phytoestrogens
°
Selected
organophosphate
pesticides
°
Organochlorine
pesticides
°
Carbamate
pesticides
°
Herbicides
°
Pest
repellents
and
disinfectants
See
Attachment
#
1
for
a
complete,
detailed
list.

CDC
has
solicited
nominations
for
chemicals
or
categories
of
chemicals
to
include
in
future
reports
(
Federal
Register,
Vol.
67,
Nol194,
October
7,
2002,
pages
62477­
8).
Sample
Locations:
The
data
are
representative
of
the
noninstitutional,
civilian
U.
S.
population.
The
survey
design
provides
estimates
for
the
U.
S.
population.
The
current
design
does
not
permit
estimates
to
be
made
on
a
state­
by­
state
or
city­
by­
city
basis.

Sample
Design:
Chemicals
and
their
metabolites
were
measured
in
both
blood
and
urine
samples.
For
urine
measurements,
data
are
shown
for
both
the
concentration
in
urine
and
the
concentration
corrected
for
urine­
creatinine
level.
The
report
presents
exposure
data
for
the
U.
S.
population
divided
into
age,
gender,
and
race/
ethnicity
groups.

Study
Duration:
The
first
report
was
issued
in
March
2001.
The
second
report
was
released
in
January
2003
and
covers
the
2­
year
period
from
1999­
2000.
Future
reports
are
expected
to
be
released
every
two
years.

Results:
The
report
presents
tables
of
descriptive
statistics
on
the
distribution
of
blood
or
urine
levels
for
each
environmental
chemical.
Statistics
include
geometric
means
and
percentiles
with
confidence
intervals.

Attachment
#
2
shows
the
results
for
Mercury.

Contact:
Centers
for
Disease
Control
and
Prevention,
National
Center
for
Environmental
Health,
Division
of
Laboratory
Science;
1­
866­
670­
6052;
e­
mail:
ncehdls@
cdc.
gov.

Short­
term
Followup:
None.

Long­
term
Followup:
Any
pollutants
we
identify
as
being
of
concern
should
be
checked
to
see
if
they
are
included
in
the
NHANES
and
what
the
results
were.
Alternatively,
we
might
be
able
to
link
the
pollutants
with
potential
sources
once
the
pollution/
industry
crosswalk
is
completed.
Attachment
1
Chemicals
in
the
NHANES
Report
Metals
(
13)
(
all
in
urine)
Lead
(
also
in
blood)
Cadmium
(
also
in
blood)
Mercury
(
also
in
blood)
Cobalt
Uranium
Antimony
Barium
Beryllium
Cesium
Molybdenum
Platinum
Thallium
Tungsten
Polyaromatic
Hydrocarbons
(
PAHs)
(
14)
1­
Hydroxybenz[
a]
anthracene
3­
Hydroxybenz[
a]
anthracene
1­
Hydroxybenzo[
c]
phenanthrene
2­
Hydroxybenzo[
c]
phenanthrene
3­
Hydroxybenzo[
c]
phenanthrene
3­
Hydroxychrysene
6­
Hydroxychrysene
3­
Hydroxyfluoranthene
2­
Hydroxyfluorene
3­
Hydroxyfluorene
1­
Hydroxyphenanthrene
2­
Hydroxyphenanthrene
3­
Hydroxyphenanthrene
1­
Hydroxypyrene
Tobacco
Smoke
(
1)
Cotinine
Phthalates
(
7)
Mono­
ethyl
phthalate
Mono­
butyl
phthalates
Mono­
benzyl
phthalate
Mono­
cyclohexyl
phthalate
Mono­
2­
ethylhexyl
phthalate
Mono­
n­
octyl
phthalate
Mono­
isononyl
phthalate
Phytoestrogens
(
6)
Daidzein
Enterodiol
Enterolactone
Equol
Genistein
O­
Desmethylangolensin
Polychlorinated
Dibenzo­
p­
dioxins,
Polychlorinated
Dibenzofurans,
and
Coplanar
Polychlorinated
Biphenyls
(
18)
1,2,3,4,6,7,8,9­
Octachlorodibenzo­
p­
dioxin
(
OCCD)
1,2,3,4,6,7,8­
Heptachlorodibenzo­
p­
dioxin
(
HpCDD)
1,2,3,6,7,8­
Hexachlorodibenzo­
p­
dioxin
(
HxCDD)
1,2,3,7,8,9­
Hexachlorodibenzo­
p­
dioxin
(
HxCDD)
1,2,3,7,8­
Pentachlorodibenzo­
p­
dioxin
(
PeCDD)
2,3,7,8­
Tetrachlorodibenzo­
p­
dioxin
(
TCDD)
1,2,3,4,6,7,8,9­
Octachlorodibenzofuran
(
OCDF)
1,2,3,4,6,7,8­
Heptachlorodibenzofuran
(
HpCDF)
1,2,3,4,7,8­
Hexachlorodibenzofuran
(
HxCDF)
1,2,3,6,7,8­
Hexachlorodibenzofuran
(
HxCDF)
1,2,3,7,8,9­
Hexachlorodibenzofuran
(
HxCDF)
1,2,3,7,8­
Pentachlorodibenzofuran
(
PeCDF)
2,3,4,6,7,8­
Hexachlorodibenzofuran
(
HxCDF)
2,3,4,7,8­
Pentachlorodibenzofuran
(
PeCDF)
2,3,7,8­
Tetrachlorodibenzofuran
(
TCDF)
3,3',
4,4',
5,5'­
Hexachlorobiphenyl
(
PCB
169)
3,3',
4,4',
5­
Pentachlorobiphenyl
(
PCB
126)
3,4,4',
5­
Tetrachlorobiphenyl
(
PCB
81)

Polychlorinated
Biphenyls
(
22)
2,4,4'­
Trichlorobiphenyl
(
PCB
28)
2,2',
5,5'­
Tetrachlorobiphenyl
(
PCB
52)
2,3',
4,4'­
Tetrachlorobiphenyl
(
PCB
66)
2,4,4',
5­
Tetrachlorobiphenyl
(
PCB
74)
2,2',
4,4',
5­
Pentachlorobiphenyl
(
PCB
99)
2,2',
4,5,5'­
Pentachlorobiphenyl
(
PCB
101)
2,3,3',
4,4'­
Pentachlorobiphenyl
(
PCB
105)
2,3',
4,4',
5­
Pentachlorobiphenyl
(
PCB
118)
2,2',
3,3',
4,4'­
Hexachlorobiphenyl
(
PCB
128)
2,2',
3,4,4',
5'­
Hexachlorobiphenyl
(
PCB
138)
2,2',
3,4',
5,5'­
Hexachlorobiphenyl
(
PCB
146)
2,2',
4,4',
5,5'­
Hexachlorobiphenyl
(
PCB
153)
2,3,3',
4,4',
5­
Hexachlorobiphenyl
(
PCB
156)
2,3,3',
4,4',
5'­
Hexachlorobiphenyl
(
PCB
157)
2,3',
4,4',
5,5'­
Hexachlorobiphenyl
(
PCB
167)
2,2',
3,3',
4,4',
5­
Heptachlorobiphenyl
(
PCB
170)
2,2',
3,3',
4,5,5'­
Heptachlorobiphenyl
(
PCB
172)
2,2',
3,3',
4,5',
6'­
Heptachlorobiphenyl
(
PCB
177)
2,2',
3,3',
5,5',
6­
Heptachlorobiphenyl
(
PCB
178)
2,2',
3,4,4',
5,5'­
Heptachlorobiphenyl
(
PCB
180)
2,2',
3,4,4',
5',
6­
Heptachlorobiphenyl
(
PCB
183)
2,2',
3,4',
5,5',
6­
Heptachlorobiphenyl
(
PCB
187)

Organophosphate
Pesticides:
Dialkyl
Phosphate
Metabolites
(
6)
Dimethylphosphate
Dimethylthiophosphate
Dimethyldithiophosphate
Diethylphosphate
Diethylthiophosphate
Diethyldithiophosphate
Organophosphate
Pesticides:
Specific
Metabolites
(
4)
Malathion
dicarboxylic
acid
para­
Nitrophenol
3,5,6­
Trichloro­
2­
pyridinol
2­
Isopropyl­
4­
methyl­
6­
hydroxypyrimidine
Organochlorine
Pesticides
(
13)
Hexachlorobenzene
Hexachlorocylclohexane
Beta­
hexachlorocyclohexane
Gamma­
hexachlorocyclohexane
Dichlorodiphenyltrichloroethane
p,
p'­
DDT
p,
p'­
DDE
o,
p'­
DDT
Oxychlordane
trans­
Nonachlor
Heptachlor
epoxide
Mirex
Pentachlorophenol
Trichlorophenols
2,4,5­
Trichlorophenol
2,4,6­
Trichlorophenol
Carbamate
Pesticides
(
3)
1­
Naphthol
2­
Isopropoxyphenol
Carbofuranphenol
Herbicides
(
5)
2,4,5­
Trichlorophenoxyacetic
acid
2,4­
Dichlorophenoxyacetic
acid
2,4­
Dichlorophenol
Atrazine
mercapturate
Alachlor
mercapturate
Pest
Repellents
and
Disinfectants
(
4)
2­
Naphthol
2,5­
Dichlorophenol
N,
N­
diethyl­
3­
methylbenzamide
ortho­
phenylphenol
Attachment
2
Excerpt
from
the
Second
National
Report
on
Human
Exposure
to
Environmental
Chemicals
Mercury
CAS
No.
7439­
97­
6
General
Information
Mercury
is
a
naturally
occurring
metal
that
has
metallic,
inorganic,
and
organic
forms.
Metallic
mercury
(
quicksilver)
is
a
shiny,
silver­
white
liquid.
Metallic
elemental
mercury
is
used
to
produce
chlorine
gas
and
caustic
soda.
It
also
can
be
used
in
detonating
devices,
cosmetics,
pharmaceuticals,
pesticides,
blood
pressure
devices,
electrical
equipment
(
e.
g.,
thermostats
and
switches),
thermometers,
dental
fillings,
and
batteries.
Spills
of
metallic
mercury
can
volatilize
into
the
air
and
be
inhaled.
Elemental
mercury
is
poorly
absorbed
from
the
gastrointestinal
tract.
Vaporization
of
mercury
from
dental
amalgams
also
contributes
to
exposure
(
Ritchie
et
al.,
2002).

Inorganic
mercury
exists
in
two
oxidative
states
(
mercurous
and
mercuric)
and
combines
with
other
elements,
such
as
chlorine
(
mercuric
chloride),
sulfur,
or
oxygen,
to
form
inorganic
mercury
compounds
or
salts.
Inorganic
mercury
enters
the
air
from
the
mining
of
ore
deposits,
the
burning
of
coal,
and
the
incineration
of
waste.
It
also
enters
the
water
or
soil
from
natural
deposits,
disposal
of
wastes,
and
volcanic
activity.

Mercury
can
combine
with
organic
compounds
(
e.
g.,
methyl
mercury,
phenyl
mercury,
merthiolate).
In
mercurycontaminated
water
or
soil,
microorganisms
can
organify
mercury
into
methyl
mercury,
which
concentrates
in
the
food
chain.
Fish
consumption
is
the
primary
source
of
methyl
lmercury
exposure
in
people.

The
health
effects
of
mercury
are
diverse
and
can
depend
on
the
form
of
the
mercury
encountered
and
the
severity
and
length
of
exposure.
With
large
acute
exposures
to
elemental
mercury
vapor,
the
lungs
may
be
injured.
At
levels
below
those
that
cause
lung
injury,
low­
dose
or
chronic
inhalation
may
affect
the
nervous
system.
Symptoms
include
weakness;
fatigue;
loss
of
weight
(
with
anorexia);
gastrointestinal
disturbances;
salivation;
tremors;
and
behavioral
and
personality
changes,
including
depression
and
emotional
instability.

Exposure
to
inorganic
mercury
usually
occurs
by
ingestion.
The
most
prominent
effect
is
on
the
kidneys,
where
mercury
accumulates,
leading
to
tubular
necrosis.
In
addition,
there
may
be
an
irritant
or
corrosive
effect
on
the
gastrointestinal
tract
involving
stomatitis,
ulceration,
diarrhea,
vomiting,
and
bleeding.
Psychomotor
and
neuromuscular
effects
also
may
occur.

Organic
mercury
is
more
toxic
than
inorganic
mercury.
The
effects
of
organic
mercury
include
changes
in
vision,
sensory
disturbances
in
the
arms
and
legs,
cognitive
disturbances,
dermatitis,
and
muscle
wasting.
The
developing
nervous
system
of
the
fetus
and
infants
are
considered
to
be
susceptible
to
the
effects
of
methyl
mercury
as
measured
by
neurobehavioral
testing
in
population
studies
(
National
Academy
of
Sciences,
2000).
Information
about
external
exposure
(
environmental
levels)
and
health
effects
is
available
at
the
EPA
IRIS
Web
site
at
http://
www.
epa.
gov/
iris
and
from
ATSDR
at
http://
www.
atsdr.
cdc.
gov/
toxprofiles.
Interpreting
Blood
and
Urine
Mercury
Levels
Reported
in
the
Tables
Blood
mercury
levels
were
measured
in
a
subsample
of
NHANES
participants
aged
1­
5
years
and
in
females
aged
16­
49
years.
Urine
mercury
levels
were
measured
in
a
subsample
of
females
aged
16­
49
years.
Subsamples
were
randomly
selected
within
the
specified
age
ranges
to
be
a
representative
sample
of
the
U.
S.
population.
The
measurement
of
total
blood
mercury
includes
both
inorganic
and
organic
forms.
In
the
general
population,
total
blood
mercury
is
due
mostly
to
the
dietary
intake
of
organic
forms,
particularly
methyl
mercury.
Urinary
mercury
mostly
comprises
inorganic
mercury,
since
little
organic
mercury
is
excreted
in
the
urine.
These
distinctions
can
assist
in
the
interpretation
of
the
meaning
of
elevated
mercury
blood
levels
in
people.
Finding
a
measurable
amount
of
mercury
in
blood
or
urine
does
not
mean
that
the
level
of
mercury
causes
an
adverse
health
effect.

Total
blood
mercury
levels
in
this
Report
were
well
below
occupational
thresholds
of
concern.
ACGIH
recommends
that
the
blood
inorganic
mercury
of
workers
not
exceed
15
µ
g/
L
and
that
urine
values
not
exceed
35
µ
g/
gram
creatinine.
Information
about
the
biological
exposure
indices
(
BEI)
is
provided
here
for
comparison,
not
to
imply
that
the
BEI
is
a
safety
level
for
general
population
exposure.
The
measurement
of
urinary
protein
excretion
for
assessment
of
early
kidney
tubular
damage
is
also
recommended.
Roels
et
al.
(
1999)
evaluated
the
utility
of
urinary
mercury
concentrations
in
assessing
renal
injury.
They
concluded
that,
to
prevent
cytotoxic
and
functional
renal
effects,
urinary
mercury
levels
should
not
exceed
50
µ
g/
gram
creatinine.

Blood
mercury
levels
in
this
NHANES
1999­
2000
subsample
are
consistent
with
levels
found
in
other
population
studies.
In
Germany,
the
geometric
mean
for
blood
mercury
was
0.58
µ
g/
L
in
all
4,645
participants
and
was
0.33
µ
g/
L
for
children
6­
14
years
old
(
Becker
et
al.,
1998).
During
the
years
1996
through
1998,
Benes
et
al.
(
2000)
studied
1,216
blood
donors
(
896
males
and
320
females;
average
age
33
years)
and
758
children
(
average
age
9.9
years).
They
found
concentrations
of
mercury
in
blood
for
adults
(
medians)
of
0.78
µ
g/
L
and
in
the
juvenile
population
of
0.46
µ
g/
L.
Total
blood
mercury
is
known
to
increase
with
greater
fish
consumption
(
Grandjean
et
al.,
1995;
Mahaffey
and
Mergler
1998;
Sanzo
et
al.,
2001;
Dewailly
et
al.,
2001)
and
with
the
number
of
teeth
filled
with
mercury­
containing
amalgams
(
Becker
et
al.,
1998).
The
levels
reported
in
this
NHANES
1999­
2000
subsample
for
maternal­
aged
females
were
below
levels
associated
with
in
utero
effects
on
the
fetus,
or
with
effects
in
children
and
adults
(
National
Academy
of
Sciences,
2000).

Geometric
mean
blood
levels
of
the
demographic
groups
were
compared
after
adjustment
for
the
covariates
of
race/
ethnicity,
age,
gender,
log
serum
cotinine
and
urinary
creatinine.
Females
aged
16­
49
years
had
blood
mercury
levels
that
were
more
than
double
those
of
children
aged
1­
5
years.
Among
children
1­
5
years
old,
girls
had
higher
values
than
boys.
In
addition,
non­
Hispanic
whites
had
lower
blood
mercury
levels
than
either
non­
Hispanic
blacks
or
Mexican
Americans.
Among
maternal­
aged
women
(
16­
49
years
old),
blood
mercury
levels
in
non­
Hispanic
blacks
were
higher
than
levels
in
non­
Hispanic
whites
and
Mexican
Americans.

In
this
Report,
no
differences
existed
between
racial/
ethnic
groups
for
urinary
mercury
levels.
Use
of
certain
mercury­
containing
cosmetic
creams
can
increase
urine
mercury
levels
slightly
(
McRill
et
al.,
2000).

These
data
provide
physicians
with
a
reference
range
so
that
they
can
determine
whether
people
have
been
exposed
to
higher
levels
of
mercury
than
those
found
in
the
general
population.
These
data
will
also
help
scientists
plan
and
conduct
research
about
mercury
exposure
and
health
effects.

For
Tables
8,
9,
and
10,
see
http://
www.
cdc.
gov/
exposurereport/
pdf/
SecondNER.
pdf,
pages17,
18,
and
19.