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Environmental
Health
Perpectives
Vol.
89,
pp.
125-135,
1990
Methods
for
Reducing
Lead
Exposure
in
Young
Children
and
Other
Risk
Groups:
An
Integrated
Summary
of
a
Report
to
the
U.S.
Congress
on
Childhood
Lead
Poisoning
by
Paul
Mushak*
and
Annemarie
F.
Crocettit
As
part
of
a
Congressionally
mandated
report
on
U.S.
childhood
lead
poisoning
prepared
by
the
Federal
govem-
ment
(U.S.
Agency
for
Txic
Substances
and
Disease
Registry
[ATSDR]),
the
authors
have
analyzed
the
relative
effectiveness
of
measures
to
reduce
source-specific
lead
exposure
of
U.S.
children.
An
integrated
overview
of
this
analysis
is
presented
in
this
article.
Two
national
actions,
the
Federally
mandated
phasedown
of
lead
in
gasoline
by
the
U.S.
Environmental
Protection
Agency
and
the
voluntary
phasedown
of
lead
use
in
domestic
food
can
production,
are
examples
of
centrally
directed
initiatives
that
have
been
relatively
successful
in
limiting
childhood
lead
exposure
in
the
U.S.
Efforts
to
abate
lead-based
paint
exposure
of
children
have
largely
failed.
This
is
especially
true
for
the
nations
21
million
residential
units
with
the
highest
lead
content
paint.
Similar-
ly,
abatement
of
lead
exposure
from
contaminated
dusts
and
soils
has
generally
been
unsuccessful.
Comprehensive
measures
to
reduce
lead
exposure
from
drinking
water
in
residences
and
public
facilities,
e.g.,
elementary
schools,
are
only
now
being
promulgated
or
implemented.
The
full
extent
of
their
effectiveness
remains
to
be
demonstrated.
There
are
many
miscellaneous
but
potentially
severe
exposure
sources
that are
difficult
to
control
but
require
attention,
such
as
poorly
glazed
foodware
and
ethno-specific
preparations.
Introduction
In
mandating
a
report
to
Congress
(1)
on
U.S.
childhood
lead
poisoning,
Section
118(f)
of
the
1986
Superfund
Amend-
ments
and
Reauthorization
Act
(SARA)
directed
the
Federal
government's
Agency
for
Toxic
Substances
and
Disease
Registry
(ATSDR)
to
examine
methods
and
alternatives
for
reducing
environmental
lead
exposure
in
young
children
in
the
U.S.
This
paper
concerns
Chapter
IX
of
ATSDR's
re-
port
to
Congress
(2),
with
some
further
updating.
This
topic
encompasses
many
environmental
and
social
issues,
and
only
a
limited
number
of
them
could
be
discussed
in
the
report
to
Congress.
One
clear
message
from
a
number
of
chapters
in
the
report
to
Congress
(1)
is
that
significant
childhood
lead
expo-
sure
persists
for
a
number
of
lead
sources
and
pathways.
For
other
sources,
specific
measures
with
major
conse-
*Department
of
Pathology
(Adjunct),
University
of
North
Carolina
at
Chapel
Hill,
811
Onslow
Street,
Durham,
NC
27705.
tDepartment
of
Community
Medicine
(Adjunct),
New
York
Medical
College,
31
Union
Square
West,
New
York,
NY
10003.
Address
reprint
requests
to
P.
Mushak,
811
Onslow
Street,
Durham,
NC
27705.
quences
for
exposure
control
have
been
put
in
place
in
the
U.S.
These
measures
are
helping
to
reduce
some
of
the
original
levels
of
exposure
and
toxicity
in
identifiable
seg-
ments
of
populations
at
special
risk.
Lead
exposure
abatement
can
be
examined
with
regard
to
various
levels
of
effectiveness.
Is
it
simply
the
lowering
of
population
blood
lead
(PbB)
levels
below
some
value
asso-
ciated
with
an
adverse
health
risk?
Alternatively,
should
reducing
population
exposure
also
provide
some
margin
of
safety?
This
safety
margin
is
desirable
for
obvious
reasons,
not
the
least
of
which
is
the
strikingly
small
size
of
this
margin
in
many
individuals,
i.e.,
between
PbB
levels
in
many
sub-
jects
and
levels
at
which
health
effects
are
seen.
Future
in-
formation
may
well
cause
further
downward
revisions
in
ac-
ceptable
levels
of
PbB,
providing
a
second
argument
for
an
adequate
current
safety
margin.
Exposure
prevention
is
described
here
as
either
primary
or
secondary
preventive
measures.
Tertiary
components
of
exposure
prevention,
as
defined
by
others,
are
presented
in
this
article
as
a
part
of
secondary
methods.
Specific
com-
ponents
of
each
type
of
exposure
prevention
method
are
depicted
in
Table
1.
MUSHAK
AND
CROCE
TTI
Table
1.
Categorical
tabulation
of
components
of
primary
and
secondary
prevention
of
lead
exposure
in
children
and
related
U.S.
risk
groups.
Type
of
prevention
method
Components
of
method
Primary
Environmental
Lead
in
paint
Lead
in
ambient
air
Leaded
gasoline
combustion
Point
source
emissions
Lead
in
dusts/soils
Lead
in
drinking
water
Lead
in
foods
Environmental/biological
Source
controls
augmented
by
community-nutrition
interventions,
i.e.,
nutritional
supplementations,
for
calcium
and
iron
Secondary
Environmental
Case
finding
Screening
programs
Environmental
follow-up
Event-specific
exposure
abatement
Environmental/biological
Nutritional
assessment
and
follow-
up
on
ad
hoc
identification
basis
Extra-environmental
Legal
actions
and
strictures
In
the
case
of
lead
exposure,
primary
prevention
involves
both
preventing
entry
of
the
lead
source
and
its
removal,
reduction,
or
avoidance
of
contact
once
present.
By
con-
trast,
secondary
methods
of
prevention
are
basically
reac-
tive
in
nature,
i.e.,
they
comprise
a
cluster
of
responses
to
existing
and
identified
problems.
Primary
and
secondary
prevention
strategies
are
further
differentiated
as
to
either
environmental
exposure
exclu-
sively
or
environmental
control
in
tandem
with
biological
approaches.
The
latter
involve
reduction
of in
vivo
exposure
and
toxicity
risk.
In
lead
exposure,
for
example,
nutritional
factors
such
as
adequate
iron,
calcium,
and
phosphorus
can
reduce,
to
some
degree,
lead
absorption
from
the
gastro-
intestinal
tract
in
children.
Optimizing
child
nutrition,
however,
is
no
substitute
for
environmental
exposure
abatement.
Examples
of
primary
and
secondary
prevention
of
lead
exposure
are
found
in
the
case
of
leaded
paint.
The
ban-
ning
of
toxic
levels
of
lead
in
newly
manufactured
paint,
in
1977,
by
the
U.S.
Consumer
Product
Safety
Commis-
sion
illustrated
primary
prevention
of
lead
exposure.
This
action,
while
a
primary
prevention
initiative,
did
nothing
for
the
enormous
reservoir
of
leaded
paint
in
tens
of
millions
of
U.S.
dwellings.
This
exposure
threat
therefore
requires
combined
primary
and
secondary
approaches.
Prinary
steps
include
leaded
paint
abatement
and
preventing
the
flaking
of
old
paint.
Screening
for
actual
leaded
paint
exposure,
by
contrast,
is
considered
secondary
prevention,
as
are
steps
to
minimize
child
contact
with
existing
leaded
paint.
Past
and
current
problems
with
lead
as
a
U.S.
public
health
problem
are
traceable
to
failures
in
primary
preven-
tion
mechanisms.
For
example,
adequate
safety
assess-
ments
for
leaded
paints
and
leaded
gasoline,
as
now
commonly
defined,
were
not
originally
applied
to
these
sources.
According
to
Rosner
and
Markowitz
(3)
and
Hamilton
et
al.
(4),
who
examined
the
use
of
leaded
gasoline
at
either
end
of
a
60-year
span,
the
introduction
of
lead
alkyls
as
a
gasoline
antiknock
additive
was
permitted
in
the
absence
of
any
credible
public
health
risk
assessment.
Present
U.S.
regulatory
practices
would
not
permit
very
many
uses
of
lead
if
it
were
in
new
products.
Primary
Prevention
Measures
for
Lead
Exposure
This
section
deals
with
the
environmental
control
of
lead
in
paint,
lead
in
the
atmosphere
from
leaded
gasoline
and
stationary
sources,
dusts
and
soils,
water
and
food.
It
also
includes
use
of
both
environmental
and
nutritional
measures.
Primary
Prevention
Using
Environmental
Measures
Primary
prevention
as
applied
to
lead
exposure
to
various
sources
has
actually
been
a
hybrid
of
conventional
primary
prevention
measures
and
post
hoc
efforts
that
resemble
secondary
prevention
approaches.
Lead
in
Paint.
National
and
other
regulatory
actions
to
control
leaded
paint
exposure
were
only
instituted
after
childhood
lead
poisoning
cases
associated
with
leaded
paint
ingestion
had
been
recognized
(5).
Control
actions
are
divided
into
Federal
and
non-Federal
controls.
Federal
Actions
in
Preventing
Paint
Lead
Exposure
in
Young
Children.
Federal
action
for
primary
prevention
of
childhood
leaded
paint
exposure
are
mainly
those
of
the
U.S.
Department
of
Housing
and
Urban
Development
(HUD)
and
the
U.S.
Consumer
Product
Safety
Commis-
sion
(CPSC).
These
actions
were
mandated
by
Congress
through
diverse
legislation.
The
principal
role
of
CPSC
in
lead
control
was
to
man-
date
reduction
of
lead
levels
in
paint
to
0.06%
in
1977.
This
measure
only
affected
the
rate
of
new
input
of
leaded
paint
into
U.S.
housing
and
public
building
stock,
since
CPSC's
mandate
does
not
address
the
preexisting
paint
lead
burden
in
U.S.
housing
stock,
nor
does
it
cover
paints
not
sold
in
interstate
commerce.
Reduction
to
a
level
of
0.06%
fol-
lowed
an
unofficial
voluntary
restriction
by
the
manufac-
turers
themselves
to
a
1%
lead
content
in
the
late
1950s.
However,
between
the
1950s
and
1977,
paint
stocks
with
lead
in
excess
of
this
level
continued
to
be
produced
(5).
This
level
of
1%
(as
dry
solid)
still
amounted
to
10,000
ppm
lead,
a
level
sufficient
to
produce
elevated
risk
of
systemic
exposure
(2).
A
lingering
problem
with
leaded
paint
is
the
disposition
of
old
retail
stock
that
has
high
lead
content.
CPSC,
for
example,
is
not
authorized
to
act against
salvage,
close-
out,
and
bankruptcy
sales
if
stock
was
manufactured
before
the
June
22,
1977,
effective
date
of
the
0.06%
standard.
Therefore,
some
high
lead
paints
may
still
be
in
retail
channels.
The
Connecticut
Department
of
Consumer
Protection,
for
example,
has
noted
that
lead-based
paint
can
reach
the
126
REDUCING
CHILDHOOD
LEAD
EXPOSURE
market
in
higher
amounts
than
expected
(Communication
of
Department
of
Consumer
Protection,
State
of
Connecti-
cut,
to
Jane
S.
Lin-Fu,
HHS,
September
17,
1985).
Con-
necticut
found
lead-based
paint
that
was
over
22
years
old
on
retail
shelves
during
1985.
Discount
and
salvage
outlets
will
have
bought
close-out
inventories
and
kept
lead-based
paint
in
the
consumer
pipe-
line
to
some
extent.
Of
concern
also
is
the
fact
that
paint
producers
are
permitted
to
market
a
"sludge"
paint
from
new
materials
plus
residues
from
vats.
If
these
residues
are
from
lead-containing
industrial
products,
then
the
ulti-
mate
lead
level
in
the
sludge
paint
may
exceed
the
CPSC
limit
of
0.06%.
In
contrast
to
CPSC's
role,
that
of
HUD
is
directed
to
leaded
paint
already
present
in
either
public
housing
or
hous-
ing
involving
Federal
assistance.
However,
HUD
did
restrict
the
use
of
high
lead
levels
in
paints
in
housing
stock
under
its
jurisdiction.
The
1971
Lead-Based
Paint
Poisoning
Pre-
vention
Act
(LPPPA)
(6)
authorized
HUD
action
to
prohibit
the
use
of
leaded
paint
in
Federal
or
Federally
assisted
con-
struction
or
rehabilitation;
relevant
HUD
regulations
were
adopted
in
1972.
A
major
statutory
step
forward
in
HUD's
responsibilities
was
mandated
in
Section
302
of
the
Act
(6),
added
in
1973,
which
required
HUD
to
set
up
procedures
for
leaded
paint
abatement
in
existing
housing
stock.
Here
also,
junisdiction
was
limited
to
Federally
connected
housing.
In
1973
and
again
in
1976,
HUD
acted
in
two
ways
under
provisions
of
Section
302:
warnings
to
purchasers
and
ten-
ants
of
HUD-associated
housing
as
to
"immediate
hazard"
in
housing
built
before
1950,
and
prohibiting
lead-based
paint
at
a
level
above
0.5%
(prior
to
the
0.06%
level
as
of
June
22,
1977).
Recently,
HUD
has
become
more
involved
as
a
result
of
the
outcome
of
1983
Federal
court
action
(7).
This
action
successfully
challenged
HUD
regulations
so
as
to
include
essentially
all
lead-painted
surfaces
as
an
"immed-
iate
hazard"
rather
than
just
those
conditions
associated
with
deteriorating
painted
surfaces.
HUD
has
promulgated
three
rules
that
extend
its
activities
in
this
area:
a)
lead
paint
hazard
elimination
in
public
and
Indian
housing
(8);
b)
lead
paint
hazard
elimination
in
FHA
single-
and
multifamily
units
and
Section
8
housing/housing
voucher
and
rehabilitation,
FHA
single-
and
multif
prop-
erty
disposition
(foreclosure)
programs
(9),
and
c)
lead
paint
hazard
elimination
in
various
community-based
Federal
grant
and
related
programs
(10).
Collectively,
these
new
actions
address
virtually
the
full
spectrum
of
U.S.
housing
activity
in
which
HUD
has
some
assistance
role.
However,
no
Federal
action
exists
to
reach
directly
into
fully
private
sector
housing
except
for
control
of
the
lead
level
in
new
paint
offered
for
sale
(see
above).
The
new
regulation
concerning
public
and
Indian
housing
includes
required
inspections
for
defective
paint
surfaces
in
units
with
children
less
than
7
years
old
and
require
inspections
for
chewable
and
defective
surfaces
if
a
child
has
an
elevated
PbB
level.
The
test
threshold
for
paint
lead
in
all
cases
is
1
mg/cm2
lead.
These
regulations
also
require
accurate
use
of
lead
detectors
by
competent
operators.
Hazard
abatement,
i.e.,
leaded
paint
removal,
is
required
when
a
child
is
identified
with
an
elevated
PbB
in
the
dwell-
ing,
in
common
areas,
or
in
public
child
care
facilities
within
control
of
public
housing.
HUD
activity
in
FHA-supported
and
similar
housing
in
these
regulations
had
a
1973
construction
cutoff,
i.e.,
hous-
ing
built
in
this
year
and
earlier
is
covered
under
the
action,
but
this
date
was
subsequently
changed
to
1978.
Inspection
for
defective
surfaces,
as
with
the
public/Indian
housing
action,
does
not
require
X-ray
fluorescence
analysis,
but
the
chewable,
protruding
surfaces
do.
Further
details
can
be
found
in
the
Federal
Register
notice
(9).
Testing
and
abatement
actions
for
FHA-assisted
housing
are
triggered
by
change
in
ownership and
continuation
of
Federal
mort-
gage
insurance.
If
a
leaded
paint-contaminated
unit
remains
in
its
present
ownership
or
is
bought
through
non-Federal
financing,
then
these
requirements
do
not
apply.
The
third
action
requires
that
Community
Development
Block
Grant,
Urban
Development
Action
Grant,
Secretary's
Fund,
Section
312
Rehabilitation
Loan,
Rental
Rehabilitation,
and
Urban
Homesteading
Program
applicants
must
carry
out
lead
paint
analysis
and
abatement
steps
in
order
to
receive
funds
within
the
programs.
Both
this
cluster
of
HUD
community
grant
programs
and
those
involving
FHA-related
assistance
place
abatement
costs
primarily
on
the
private
sectors
involved
in
the
housing
transactions.
Most
recently,
HUD
has
taken
further
steps
toward
paint
hazard
elimination
(11)
as
directed
by
Section
566
of
the
Housing
and
Community
Development
Act
of
1987
(12).
This
rulemaking
amends
a
number
of
current
regulations,
changes
definition
of
abatable
surfaces
to
include
exterior
as
well
as
interior
surfaces,
and
advances
the
construction
cutoff
date
to
1978
from
1973
(see
above).
Finally,
and
as
required
by
PL
100-242
(12),
HUD
must
report
to
Con-
gress
by
December
1989
on
safe
and
effective
abatement
methods
and
a
comprehensive
inspecting
and
paint
lead
removal
plan.
While
these
recent
actions
suggest
a
more
concerted
effort
to
attack
the
leaded
paint
hazard,
quantification
of
the
likely
or
estimated
impact
of
the
three
rulemaking
actions
is
important.
Table
2
provides
estimates
of
the
number
of
units
and
associated
abatement
costs
in
public
housing,
at
a
paint
lead
removal
action
level
of
1
mg/cm
(13).
About
308,000
units
are
estimated
to
require
abate-
ment
across
all
unit
age
categories
with
an
aggregate
cost
of
$380.1
million
in
1986
dollars.
This
figure
appears
to
be
too
low.
Table
3
presents
the
estimated
number
of
units
requiring
lead
abatement
for
each
year,
1987
to
1991,
and
the
pro-
jected
cost
in
these
years
for
FHA
single-family
units
(14).
For
all
housing
ages,
171,300
units
are
estimated
to
require
abatement
for
each
of
the
5
years,
and
total
856,500
units
with
a
cost
of
about
$2
billion.
Single-family,
FHA-insured
units
are
but
one
category
in
this
particular
HUD
action.
Miller
and
Toulmin
(15)
have
estimated
that
for
1987
to
1991,
all
of
these
FHA
categories
will
involve
an
outlay
of
$2.57
billion.
Of
these
amounts,
about
95%
will
have
to
be
paid
by
buyers
and/or
sellers
in
the
private
sector.
Municipal
and
State Actions
in
Leaded
Paint
Expo-
sure.
In
1951,
the
city
of
Baltimore
prohibited
leaded
paint
use
on
interiors
of
dwelling
units
and,
in
1958,
required
war-
127
MUSHAK
AND
CROCETTI
Table
2.
Abatement
costs
and
number
of
units
for
different
site
categories
at
a
leaded
paint
threshold
of
1.0
mg/cm2
in
public
housing.a
Family
dwelling
units
Cabinet
surfaces
Housing
project
units
Common
activity
sites
Construction
Cost,
Cost,
Cost,
Cost,
year
Number
$
milions
Number
$
millions
Number
$
millions
Number
$
millions
Pre-1950
81,379
86.7
5,399
3.4
11.239
25.7
413
0.7
1950-1959
111,688
108.6
3,609
2.2
16,808
61.0
425
0.5
1960-1972
114,587
62.8
0
0
11,361
28.2
457
0.3
Total
307,654
258.1
9,008
5.6
39,408
114.9
1,295
1.5
aAdapted
from
Wallace
(13).
Number
of
units
indicated
is
48.9%
of
the
total
of
629,004,
and
total
cost
is
$380.1
million.
Table
3.
Estimated
abatement
costs
and
number
of
units
for
different
site
categories
at
a
lead
paint
threshold
of
1.0
mg/cm2
in
single-family
FHA
housing
units!
Number
of
units
Year
of
abatement
Year
built
1987 1988
1989
1990
1991
1960-1972
20,500 20,500 20,500
20,500
20,500
1950-1959
55,900
55,900
55,900
55,900 55,900
Pre-1950
94,900 94,900
94,900
94,900 94,900
Total
number
171,300
171,300 171,300
171,300 171,300
Total
cost,
$
thousands
388,400
388,400
388,400
388,400 388,400
Cumulative
cost,
$
thousands
388,400
776,800
1,165,200
1,553,600 1,942,000
aFrom
Miller
and
Toulmin
(14).
ning
labels
on
cans
of
leaded
paint
already
in
the
market
pipeline
(15).
By
that
time,
the
paint
industry
had
introduc-
ed
titanium
dioxide
as
a
substitute
pigment
for
basic
lead
carbonate
in
paint,
but
lead-based
paint
continued
to
be
made
into
the
1970s.
Retroactive
regulation
at
any
level
of
jurisdiction,
i.e.,
states
or
cities,
for
paint
lead
already
in
U.S.
housing
stock
has
been
infrequent
and
variably
enforced.
In
the
early
1970s,
Philadelphia,
PA,
had
a
pnrmary
prevention
ordinance
directed
at
removing
leaded
paint
up
to
5
feet
above
the
floor
in
any
unit
with
leaded
paint.
However,
the
city
even-
tually
discarded
such
prophylactic
removal
in
favor
of
abate-
ment
only
after
demonstrated
toxicity
in
children
who
lived
in
the
units.
Among
the
states,
a
number
have
attempted
to
attack
the
problem
by
various
lead
paint
poisoning
control
statutes.
These
have
generally
produced
mixed
results.
For
exam-
ple,
Massachusetts
first
banned
lead
in
any
unit
in
which
children
younger
than
6
years
of
age
were
living,
but
various
problems
with
landlord
cooperation
and
limited
funding
for
enforcement
resulted
in
control
limited
to
secondary
preven-
tion;
that
is,
intervention
only
after
demonstrated
instances
of
toxicity
(16).
Subsequently,
in late
1987,
Massachusetts
enacted
stronger
laws
to
strengthen
the
lead
paint
hazard
identification
and
protocols
for
lead
paint
abatement.
It
is
too
early
to
judge
their
effectiveness.
In
many
states,
there
are
large
inventories
of
old
housing
requiting
leaded
paint
removal.
Summary
statistics
provided
by
the
Commonwealth
of
Massachusetts
to
ATSDR,
shown
in
Table
4,
permit
some
observations
as
to
the
magnitude
of
the
problem
and
the
rate
of
its
remediation.
Of
interest
is
the
activity
level
of
lead
removal
programs
compared
with
the
number
of
pre-1940
housing
units,
that
is,
lead-painted
units
with
high
lead
content.
The
table
indicates
that
the
selected
cities
of
the
Commonwealth
have
a
total
of
450,339
pre-1940
units
(those
with
the
highest
lead
content).
Over
the
period
January
1982
to
June
1986,
only
2260,
or
0.5%,-
of
these
units
were
subjected
to
lead
abatement.
We
are
not
aware
of
the
level,
if
any,
of
lead
removal
carried
out
under
Massachusetts
statutory
provisions
but
occurring
out-
side
the
reported
programs.
Statutes
such
as
that
of
Massachusetts
can
be
employed
in
concerted
action
by
specific
community
groups.
For
example,
a
tract
of
high-risk,
lead-painted
housing
in
the
Jamaica
Plain
area
of
Boston
was
systematically
examined
in
1981,
the
children
involved
were
screened
for
lead
tox-
icity,
and
then
50%
of
the
suspect
housing
was
treated
to
remove
lead.
The
joint
efforts
of
the
Harvard
School
of
Public
Health,
which
did
the
community
assessment,
and
the
Legal
Aid
Society,
which
used
the
Massachusetts
statu-
tory
sanctions,
forced
landlords
to
comply
(17).
Lead
in
Ambient
Air:
Leaded
Gasoline
Combustion
and
Point
Source
Emissions.
EPA
has
had
regulatory
authority
over
the
use
of
lead
in
gasoline
since
1973
(18).
In
1975,
EPA
classified
lead
as
a
criteria
pollutant,
a
designa-
tion
reserved
for
pollutants
whose
public
impact
is
such
that
control
is
required
by
ambient
standards
rather
than
by
site-
specific
emission
controls.
Several
parallel
actions
were
Table
4.
Summary
of
total
pre-1940
lead-painted
housing
versus
deleading
activity
in
selected
Massachusetts
communities
for
1982-June
30,
1986.a
Pre-1940
Units
deleaded
in
City
unitsb
1982
1983 1984
1985
1986C
Total
Boston
179,391
221
175
136
201
152
885
Worcester
43,555
148 100
99
142
67
556
Springfield
36,239
40
41
29
34
2
146
New
Bedford
29,536
9
21
16
10
1
57
Fall
River
28,502
6
5
2
1
0
14
Somervile
26,806
9
7
1
4
9
30
Lynn
26,006
20
29
21
35
12
117
Lowell
23,356
- -
- -
-
15
Lawrence
19,916
- -
- -
-
300
Newton
18,516
0
1
1
00
2
Total
450,339
453
379
305
427
243
2260
aSummary
statistics:
childhood
lead
poisoning
prevention
program.
Commonwealth
of
Massachusetts,
as
provided
by
Cosgrove
to
ATSDR,
December
10,
1986
(2).
Communities
ranked
by
number
of
pre-1940
units
b'A
pre-1940
units
are
assumed
to
have
leaded
paint
at
significant
levels.
cTo
June
30,
1986.
dTotal
only
supplied.
128
REDUCING
CHILDHOOD
LEAD
EXPOSURE
being
pursued
in
1975
under
the
aegis
of
either
Section
108
or
109
of
the
Clean
Air
Act,
as
amended
(19),
which
authorized
the
EPA
Administrator
to
set
ambient
air
stan-
dards
for
lead.
In
addition,
Section
211(c)(1)
of
the
Act
(19)
authorizes
the
Administrator
to
"control
or
prohibit
the
manufacture
...
or
sale
of
any
fuel
additive"
if
its
emission
products
cause
or
contribute
to
"air
pollution
which
may
be
reasonably
anti-
cipated
to
endanger
the
public
health
or
welfare"
or
"will
impair
to
a
significant
degree
the
performance
of
any
emis-
sion
control
device
or
system...
in
general
use."
Since
the
mid-1970s,
the
use
of
lead
in
gasoline
declined
mainly
as
a
result
of
the
increase
of
lead-sensitive,
emission
control-equipped
vehicles
in
the
U.S.
domestic
fleet.
Na-
tional
data
are
best
illustrated
by
results
of
the
Second
Na-
tional
Health
and
Nutrition
Examination
Survey
(NHANES
II)
(20)
for
the
general
population
and
children
at
high
risk
assessed
in
U.S.
Centers
for
Disease
Control
screening
programs
(21).
The
NHANES
II
data
indicated
a
general-
ized,
cross-population
decline
in
PbB
levels
of
37%,
an
average
drop
of
about
5.4
ytg/dL
(22).
In
1978,
an
ambient
air
lead
standard
of
1.5
/1g/m3
was
promulgated-a
con-
siderable
drop
from
the
earlier
standard.
This
standard
also
provided
a
means
for
controlling
point-source
emissions
from
smelters
and
similar
operations.
In
1982,
EPA
set
forth
new
rules
(23)
that,
among
other
things,
reduced
the
lead
content
of
gasoline
to
1.1
per
liquid
gallon.
In
further
action,
effective
January
1,
1986,
EPA
revised
the
phasedown
of
lead
in
gasoline
to
0.1
g
per
liquid
gallon.
The
decline
in
gasoline
lead
from
these
actions
is
expected
to
impact
the
number
of
children
whose
PbB
levels
fall
below
certain
toxicity
risk
ceilings,
including
the
1985
CDC
action
level
of
25
Ag/dL.
Prevalence
modeling
esti-
mates
by
EPA
(24)
project
sizable
declines
in
the
numbers
of
children
with
PbB
levels
above
15,
20,
and
25
Ag/dL,
owing
to
gasoline
lead
phasedown.
EPA
is
also
examining
its
1978
lead
standard
of
1.5
/g/m3
in
ambient
air.
Any
downward
revisions
will
reduce
atmo-
spheric
inputs,
mainly
near
stationary
sources.
Controls
on
lead
input
from
mobile
and
stationary
emissions
control
new
inputs.
Populations
will
continue
to
be
at
risk for
exposure
from
lead-contaminated
dust
and
soil,
arising
from
past
air
lead
fallout
(as
well
as
from
leaded
paint
weathering
and
chalking).
Lead
in
Dusts
and
Soils.
The
principal
prevention
measures
for
lead-contaminated
dust
and
soil
exposures
have
been
directed
at
the
generators
of
lead
in
paint,
leaded
gasoline,
and
stationary
source
emitters.
Currently,
only
very
limited
regulatory
action
has
been
specifically
directed
at
controlling
lead
in
dust
and
soil.
In
the
case
of
lead-
containing
waste
sites,
Chapter
X
of
the
report
to
Con-
gress
(2)
describes
Superfund
activity
and
Appendix
F
of
the
report
lists
sites
that
are
due
for
cleanup
and
which
also
contain
lead
in
soil.
Several
factors
have
contributed
to
this
lack
of
regulation.
First,
dust
and
soil
have
not
been
traditionally
recognized
in
public
health
actions
or
policy
as
specific,
potentially
major
sources
or
pathways
of
childhood
lead
exposure.
These
sources
are
complex
and
still
require
more
precise
quantitative
characterization.
Second,
legal
and
other
societal
sanctions
that
are
not
enforced
allow
primary
contributors
such
as
leaded
paint
to
continue
to
contaminate
residential
dusts
and
soils.
One
impediment
to
regulatory
or
legal
control
of lead
in
dusts
and
soils
has
been
the
relative
paucity
of
studies
showing
how
specific
primary
contributors
quantitatively
affect
given
dust
and
soil
contamination
levels.
Duggan
and
Inskip
(25)
have
reviewed
dusts
and
soils
versus
childhood
exposure
in
detail.
Recent
reports
document
that
lead
levels
in
these
media
are
quantitatively
related
to
PbB
levels
(22).
Charney
et
al.
(26)
have
shown
that
PbB
levels
can
be
reduced
through
indoor
dust
abatement
but
only
to
a
certain
point.
Milar
and
Mushak
(27)
have
shown
a
relationship
between
work-
place
dust
inadvertently
brought
home
by
lead
battery
plant
workers
and
PbB
levels
in
their
young
children.
Similarly,
the
study
by
Ryu
et
al.
(28)
shows
household
contamination
via
secondary
transport
from
the
workplace
and
lead
transfer
to
infants.
Reports
of
the
Cincinnati,
OH,
prospective
lead
studies,
concerned
with
childhood
lead
poisoning
in
that
city,
have
shed
considerable
light
on
relationships
among
path-
ways
for
household
dust,
lead
on
the
hands
of
children,
and
socioeconomic
factors
concerning
leaded
paint
as
the
likely
primary
contributors
(29-32).
Clark
et
al.
(31)
have
shown
that
dust
lead
is
best
correlated
with
lead
on
the
hands
of
children,
and
their
results
point
to
dust
lead
abatement
as
a
key
factor
in
reducing
lead
hazards
in
housing.
The
focus
of
most
studies
to
date
has
been
lead
abatement
methods
that
are
applicable
to
individual
lead
paint-containing
units.
Field
studies
are
therefore
needed
to
provide
evi-
dence
that
macro
rather
than
micro
control
strategies
are
effective
means
of
lead
abatement
in
areas
larger
than
a
single
home
or
several
homes.
Mobility
of
lead
in
dust
and
soil
prevents
a
straightforward
application
of
methods
for
single
unit
abatement
to
a
neighborhood
or
even
larger
areas.
Additional
field
surveys
may
also
be
needed
to
define
blood
lead-source
lead
relationships.
Past
attempts
to
define
soil
and
dust
lead
in
terms
of
precise
proportional
contribu-
tions
of
paint
lead
and
airborne
lead,
when
both
input
sources
were
present,
have
been
unsuccessful
for
various
reasons.
The
1986
SARA
provides
for
the
funding
and
execution
of
demonstration
projects
to
address
the
problem
of
area-
wide
soil
(and
dust)
lead
in
urban
tracts.
In
response,
the
U.S.
EPA
has
provided
for
a
small
group
of
major
demon-
stration
projects
in
several
large
U.S.
cities,
but
results
are
still
very
preliminary.
Lead
in
Drinking
Water.
EPA
is
required
by
the
1974
Safe
Drinking
Water
Act
(SDWA)
(33)
to
set
drinking
water
standards
with
two
levels
of
protection,
labeled
primary
and
secondary
standards.
The
primary
standards
for
drinking
water,
related
to
human
health,
define
contaminant
levels
in
terms
of
maximum
contaminant
level
(MCL)
or
treatment
requirements.
MCLs
are
limits
enforceable
by
law
and
are
to
be
set
as
close
as
possible
to
maximum
contaminant
level
goals
(MCLGs).
MCLGs
are
levels
essentially
determined
by
relevant
toxicologic
and
biomedical
considerations
inde-
pendent
of
how
feasible
attaining
the
levels
may
be.
In
the
1986
amendments
to
the
1974
SDWA,
EPA
was
directed
to
tighten
the
drinking
water
standards
for
various
129
MUSHAK
AND
CROCE
TTI
substances,
including
lead.
The
current
MCL
for
lead
is
50
ltg/L
of
water
(34).
In
response,
EPA
has
proposed
a
revision
of
the
MCL
from
50
to
5
lig/L
water,
measured
at
the
water
system's
outlet
rather
than
the
residential
tap
(35).
The
latter
is
principally
involved
through
the
mech-
anism
of
an
action
level,
i.e.,
>
10
,tg/L.
This
is
determined
by
a
two-tier
tap
water
sampling
in
a
community,
depend-
ing
on
population.
If
a
community's
sampling
average
exceeds
10
/ig/L,
then
corrosion
control
is
required.
Central
corrosion
control
is
an
especially
important
part
of
the
pro-
posed
changes.
In
addition,
EPA
is
also
proposing
to
con-
sider
the
removal
of
lead
service
connections
and
goose-
necks
(connections
from
the
street
line
to
house
lines).
Other
options
may
be
considered
and
selected,
and
it
is
not
possible
at
this
time
to
predict
the
final
form
of
tap
water
lead
rule
changes.
In
addition
to
the
pending
rule
on
drinking
water
lead
per
se,
the
1986
SDWA
(33)
amendments
banned
the
use
of
lead
solder
and
other
lead-containing
material
in
household
plumbing
when
residences
are
connected
to
public
water
supplies.
States
must
enforce
the
ban
or
be
subject
to
a
loss
of
Federal
grant
funds.
In
late
1988,
the
Lead
Contamination
Control
Act
of
1988
was
enacted
(36),
which
contained
both
primary
and
sec-
ondary
lead
exposure
prevention
provisions.
These
include
the
recall
of
lead-containing
public
water
coolers,
the
screen-
ing
of
school
tapwater
lead
levels,
and
assistance
to
states
for
testing
and
abating
lead
in
school
drinking
water.
EPA's
Office
of
Policy
Analysis
(37,38)
has
carried
out
a
detailed
assessment
of
lead
in
drinking
water
from
public
water
supplies.
As
noted
in
the
report
to
Congress
(1),
about
20%
of
the
population
has
tap
water
lead
levels
above
a
level
of
20
/Ag/L.
Corrosive
drinldng
water
is
quite
common
to
densely
pop-
ulated
U.S.
urban
areas,
and
the
U.S.
EPA
(37)
has
esti-
mated
that
about
62
million
Americans
consume
such
water.
A
useful
U.S.
case
study
for
primary
prevention
of
exposure
to
lead
in
drinking
water
at
the
community
level
is
that
of
the
Boston
water
system.
In
the
1970s,
the
Boston
water
authority
began
efforts
to
reduce
corrosivity,
since
many
of
the
occupied
housing
units
in
the
city
had
lead
plumb-
ing,
and
the
water
supply
was
highly
corrosive.
These
efforts
considerably
reduced
the
amount
of
lead
in
tap
water
(22,37).
The
U.S.
EPA
(37)
has
estimated
that
the
treat-
ment
to
reduce
corrosivity
costs
just
25%
of
the
value
of
the
health
benefits
realized
from
reduced
lead
exposure,
that
is,
a
benefit-to-cost
ratio
of
4:1.
While
the
Federal
actions
described
above
are
expected
to
have
an
impact
on
potential
childhood
lead
exposure,
the
final
form
of
the
proposed
changes
and
their
effective
imple-
mentation
will
determine
the
efficacy
of
lead
control
in
U.S.
water
supplies.
Lead
in
Food.
Some
quantity
of
lead
in
food
and
bever-
ages
is
ingested
by
virtually
the
entire
U.S.
child
popula-
tion.
As
noted
in
the
report
to
Congress
(1),
about
5%
of
these
children
were
estimated
to
have
a
lead
intake
high
enough
to
potentially
increase
PbB
levels
to
those
associated
with
early
health
impacts.
Consequently,
prevention
meas-
ures
that
limit
lead
exposure
from
food
are
important.
Regulating
lead
contamination
in
foods
has
been
the
responsibility
of
the
U.S.
Food
and
Drug
Administration
(FDA)
for
several
decades.
Such
control
began
with
the
identification
of
lead-containing
pesticide
residues
on
sprayed
fruits.
Collectively,
FDA
actions
from
the
1970s
onward
have
targeted
either
control
through
setting
total
lead
intake
goals
or
efforts
directed
at
known
significant
sources
of
lead
inputs
into
foods.
In
1979,
FDA
set
a
long-term
goal
of
less
than
100
jig/day
for
reducing
the
daily
lead intake
from
all
foods
for
children
1
to
5
years
old
(39).
This
is
a
maximum
permissible
intake
for
any
child
and
not
a
mean
intake
for
all
children.
To
achieve
this
goal
within
the
shortest
feasible
time,
attention
has
been
focused
on
a)
establishing
permissible
lead
resi-
dues
in
evaporated
milk
and
evaporated
sldm
milk;
b)
setting
maximum
levels
for
lead
in
canned
infant
formulas,
canned
infant
fruits
and
vegetable
juices,
and
glass-packed
infant
foods;
and
c)
establishing
action
levels
for
other
foods.
Along
with
these
activities,
FDA
attempts
to
monitor
and
enforce
controls
on
food-related
materials.
This
includes
leaching
from
pottery
glazes
and
food
utensils.
Lead
can
enter
the
food
supply
during
production,
pro-
cessing,
or
distribution.
The
U.S.
EPA
(22)
has
determined
that
during
these
activities,
the
lead
content
in
food
may
be
increased
2-
to
12-fold
over
background
levels.
Process-
ing
is
the
major
pathway
for
contamination,
especially
lead
leached
from
lead-soldered
cans.
Since
World
War
II,
the
ratio
of
lead
to
tin
in
this
soldering
material
has
remained
at
98:2.
FDA
activities,
to
a
large
extent,
consist
of
establishing
voluntary
cooperation
from
domestic
food
manufacturers
and
processors,
and
much
of
the
data
is
provided
by
the
industry.
Clearly,
lead
in
food
due
to
leaching
from
leaded
sources
has
been
significantly
reduced
(Table
5).
The
percentage
of
food
cans
that
are
lead-soldered
con-
tinues
to
decline.
Table
5
shows
the
percentages
from
1979
through
the
first
quarter
of
1986
and
also for
the
end
of
1988.
The
percentage
was
very
high
in
1979-over
90%-
but
had
declined
by
the
end
of
1988
to
approximately
6%.
Recent
data
provided
to
FDA
by
the
National
Food
Pro-
cessors
Association
(NFPA)
(40)
indicate
about
a
77%
reduction
in
lead
from
canned
food
during
the
period
1980
to
1985.
Table
5
does
not
include
imported
canned
foods;
Table
5.
Percentage
of
lead-soldered
cans
in
all
U.S.
manufactured
food
cans
from
1979
to
19858
and
1988.b
Total
food
cans,
Lead-soldered
Percent
of
Year
millions
cans,
millions
total
1979
30,543
27,576
90.29
1980
28,432
24,405
85.84
1981
27,638
20,516
74.23
1982
27,544
17,412
63.21
1983
26,942
13,891
51.56
1984
28,121
11,683
41.55
1985
27,767
8,769
31.58
1986C 6,517
1,807
27.72
1988
b
28,071
1,626
5.79
aFrom
Can
Manufacturers
Institute
data
to
U.S.
FDA
(2).
bFrom
Can
Manufacturers
Institute
(personal
communication,
April
1989).
cFirst
quarter,
1986.
130
REDUCING
CHILDHOOD
LEAD
EXPOSURE
Table
6.
Age-
and
sex-dependent
diet
lead
intakes
in
the
U.S.
at
two
time
periods
a
Lead
intake,
tg/kg/day
Change
(%)
Age,
body
weight
Sex
1982-1984
1984-1986
yg/kg/day
6-11
months,
9
kg
1.70
1.11
-0.59
(35)
2
years,
13
kg
1.60
1.00
-0.60
(37)
14-16
years,
54
kg
F
0.48
0.30
-0.18
(33)
14-16
years,
60
kg
M
0.63
0.38
-0.25
(40)
25-30
years,
60
kg
F
0.43
0.27
-0.16
(39)
25-30
years,
76
kg
M
0.48
0.29
-0.19
(40)
60-65
years,
64
kg
F
0.42
0.25
-0.17
(40)
60-65
years,
76
kg
M
0.44
0.26
-0.18
(42)
aFrom
FDA
Division
of
Toxicology,
Communication
of
Internal
Tabulations
to
ATSDR,
April
23,
1987,
based
on
Total
Diet
Study
results
(2).
Revised
Total
Diet
Study
points,
eight collections.
there
are
no
data
for
this
contribution
to
lead
in
food.
Some
changes
in
steps
causing
the
lead
contribution
from
the
food
processing
industry
were
not
taken
until
after
1981/1982.
In
the
period
1980
to
1985,
lead
in
canned
food
was
reduced
77%
(40),
and
lead
in
infant
foods
was
reduced
considerably
(41).
Recent
data
provided
by
FDA
update
the
age-dependent
reduction
found
in
data
from
the
Total
Diet
Study
between
1982
to
1984
and
1984
to
1986.
Table
6
gives
total
diet
lead
changes
with
the
percentage
decline
for
various
age-sex
categories.
Currently,
the
FDA
surveys
lead
contamination
in
the
U.S.
food
supply
by
means
of
the
Total
Diet
Study,
in
which
multiple
food
categories
are
included.
Data
for
the
ongoing
Total
Diet
Study
are
based
on
samples
that
are
still
very
small
in
relation
to
the
enormous
quantities
of
food
units
produced
and
consumed
in
the
United
States.
They
may
not
account
adequately
for
variation
by
region
and
multiplicity
of
processors.
The
types
of
food
items
selected
for
testing
also
may
not
reflect
the
variations
in
food
selection
and
con-
sumption
patterns
among
various
segments
of
the
U.S.
pop-
ulation.
The
level
of
lead
in
food
may
consequently
be
smaller
or
greater
than
indicated.
Lead
contamination
of
liquids
and
foods
by
use
of
poorly
fired
lead-glazed
pottery
can
occur,
but
it
is
not
possible
to
quantitate
the
effectiveness
of
any
FDA
controls
con-
cerning
these
objects.
Similarly,
use
of
lead-based
folk
medicine
preparations
by
various
ethnic
groups
are
quite
difficult
to
control.
Primary
Prevention
of
Exposure
Using
Combined
Environmental
and
Biological
Measures
Biological
factors
can
suppress
lead
uptake
into
the
body
or
enhance
its
excretion.
When
these
factors
are
nutrients
that
have
well-established
interactive
relationships
with
lead
uptake
and
toxicity,
such
nutrients
can
be used
to
reduce
internal
or
in
vivo
exposure.
Such
factors,
when
employed
in
a
prophylactic,
communitywide
way,
can
also
be
viewed
as
an
example
of
primary
prevention.
When
these
factors
are
exploited
on
an
ad
hoc
basis
in
children
or
famiLies
where
lead
poisoning
has
occurred,
their
use
becomes
more
a
secondary
prevention
measure.
As
discussed
by
U.S.
EPA
(22)
and
Mahaffey
et
al.
(42),
a
number
of
nutritional
factors
suppress
lead
absorption
and
toxicity
in
test
animal
and
human
populations.
However,
only
the
nutrients
iron
and
calcium
can
realistically
be
con-
sidered
in
the
context
of
preventive
community
medicine
for
high-risk
populations.
Results
of
numerous
studies
have
shown
that
both
calcium
and
iron
nutritional
status
in
young
children
is
inversely
related
to
the
lead
absorption
level.
Most
of
these
studies
are
discussed
in
the
EPA
document
(22).
A
more
recent
analysis
of
the
NHANES
II
survey
data
showed
a
significant
negative
correlation
between
calcium
status
and
PbB
levels
in
a
group
of
children
under
11
years
of
age
(42).
As
Mahaffey
(43)
has
indicated,
improving
the
nutritional
status
of
children
with
high
risk
of
exposure/toxicity
does
increase
the
effectiveness
of
environmental
lead
abatement.
On
the
other
hand,
maintenance
of
optimal
nutrition
would
mainly
shift
the
lead
level
required
for
toxicity,
i.e.,
the
dose-effect
curve,
and
would
not
eliminate
lead
toxicity
risk.
Other
nutrients
that
offset
lead
toxicity
may
not
be
par-
ticularly
useful
or
advisable
in
this
connection.
Levels
of
phosphorus
in
most
diets
seem
high
enough
to
suggest
intake
is
at
adequate
levels
in
poorer
children,
which
is
borne
out
by
the
Mahaffey
et
al.
(42)
examination
of
the
NHANES
II
data
for
children.
Vitamin
D
enhances
lead
uptake
in
the
gut,
but
its
intake
is
essential
to
health
and
cannot
be
reduced.
At
present,
no
formal
nutritional
programs
specifically
geared
to
minimizing
lead
uptake
or
toxicity
have
been
implemented
in
the
United
States.
Nutrition
monitoring
and
maintenance
to
minimize
lead
exposure
are
probably
best
done
in
a
program
of
overall
nutritional
care,
for
example,
the
Women,
Infants,
and
Children
(WIC)
nutrition
program.
The
level
of
public
funding
and
other
support
for
such
pro-
grams
determines
their
potential
in
reducing
net
lead
expo-
sure.
The
argument
can
also
be
reversed
to
show
that
increased
nutritional
impairment
for
those
at
high
risk
for
lead
poisoning
will
enhance
exposure
and
toxicity
risk
in
that
population.
It
is
well
known
that
nutrient
deficiencies
enhance
lead
uptake
and
toxicity
(22,42).
Secondary
Prevention
Measures
for
Lead
Exposure
Environmental
Lead
Control
This
section
principally
addresses
lead
screening
pro-
grams
and
other
components
of
early
intervention
in
expo-
sure
and
toxicity,
particularly
environmental
lead
source
identification
and
lead
hazard
abatement.
Screening
Programs
and
Case
Finding.
The
1971
LPPPA,
as
noted
by
Farfel
(5),
did
not
specifically
dictate
health-based
(secondary
prevention)
versus
hazard-abate-
ment
(primary
prevention)
steps
to
be
taken
to
ameliorate
lead
poisoning
in
U.S.
children.
While
Title
II
of
the
Act
(6)
authorized
grants
to
the
responsible
agency
to
remove
leaded
paint
on
a
tract
basis
in
high-risk
neighborhoods,
no
funding
for
this
purpose
was
provided.
The
Department
of
Health,
Education,
and
Welfare
emphasized
intervention,
131
MUSHAK
AND
CROCETTI
including
medical
management
if
necessary,
for
documented
toxicity.
Various
lead
screening
programs
in
high-risk
areas
of
the
United
States,
their
history,
and
their
quantitative
aspects
were
discussed
in
the
report
to
Congress
(1).
The
focus
here
is
on
their
role
as
secondary
prevention
instruments.
During
the
time
when
screening
programs
were
adminis-
tered
by
the
U.S.
CDC,
i.e.,
until
fiscal
year
1982
when
CDC
control
ended,
about
4
million
children
were
screened
nationwide,
and
about
250,000
children
were
registered
as
having
met
toxicity
risk
criteria
then
in
use.
The
screen-
ing
program
was
estimated
to
have
surveyed
about
30%
of
the
high-risk
children.
Detection
rates
for
positive
toxi-
city
through
screening
cases
are
considerably
below
those
found
in
the
NHANES
II
survey.
Reasons
for
this
difference
are
noted
in
the
report
to
Congress
(1).
Screening
and
early
detection
of
exposure
and
toxicity
have
clearly
reduced
the
rates
of
severe
lead
poisoning
(21).
However,
chronic
lead
exposure
and
lower-level
lead
tox-
icity
appear
more
resistant
to
such
secondary
prevention
approaches.
The
persistence
of
these
problems
is
predict-
able,
given
the
levels
and
types
of
unabated
exposure
remaining
in
the
United
States
(1).
In
1981,
Federal
resources
for
screening
were
put
under
the
program
of
the
Maternal
and
Child
Health
Block
Grants
to
States.
Although
the
amount
of
Federal
funds
for
lead
screening
in
such
grant
programs
to
states
was
estimated
by
one
source
to
have
been
reduced
by
25%
(5),
a
precise
figure
cannot
be
readily
given.
Allocations
of
funds
for
par-
ticular
projects
within
a
block
grant
are
determined
by
the
States,
and
data
are
not
systematically
collected
on
these
State
decisions.
Information
on
any
adverse
impact
of
this
initial
reduction
in
Federal
resources
on
screening
effectiveness
appears
to
be
inconclusive.
Although
the
total
number
of
screening
programs
in
the
nation
has
decreased
from
the
time
of
CDC
administration
(2),
in
some
States
and
localities
the
number
of
children
being
screened
has
increased
since
1981
(21,44).
Nonetheless,
loss
of
centralized
control
of
screening
criteria,
quality
control,
and
data
analysis
would
be
expected
to
slow
progress
in
both
identification
of
at-risk
children
and
the
means
for
assessing
trends
in
poisoning
risk.
In
addition,
a
detailed
study
of
data
from
Newark,
NJ,
for
a
9-year
period
showed
that
the
rate
of
positive
toxicity
cases
in
young
children
increased
about
4-fold
after
fund-
ing
for
lead
screening
and
public
education
programs
was
reduced
(45).
While
this
example
was
not
linked
to
the
change
in
screening
support
in
1981,
it
does
show
that
those
areas
that
decrease
the
efficiency
of
their
lead
screening
services
can
expect
to
experience
increases
in
the
number
of
children
with
lead
poisoning.
Lead
screening
programs,
when
supported
at
a
level
that
allows
comprehensive
screening
and
follow-up,
are
particularly
cost
effective.
This
can
be
demonstrated
by
comparing
the
costs
of
treating
children
who
are
hospitalized
because
of
lack
of
early
detec-
tion
of
exposure
in
one
community
with
the
costs
of
com-
munity
screening
programs
in
another.
According
to
O'Hara
(46),
the
cost
of
repeat
admissions
to
Baltimore
hospitals
for
19
lead-poisoned
children
in
1979
was
$141,750,
or
at
least
$300,000
in
1986
dollars
(-
$16,000
per
child).
By
comparison,
the
city
of
St.
Louis
spent
$404,453
for
its
1985-1986
program
year
(1),
and
this
allowed
testing
of
12,308
children,
of
whom
1,356
or
11.02%
tested
positive
for
lead
exposure
using
the
relevant
CDC
toxicity
risk
classifications.
Of
these
positives,
849
were
classified
as
Class
II,
445
as
Class
Ill,
and
62
as
Class
IV,
the
most
severe
level
of
toxicity
[see
report
to
Con-
gress
(1),
for
detailed
discussion
of
screening
classifications].
This
amounts
to
approximately
$300
per
child
with
early
toxicity,
or,
overall,
a
benefit:cost
ratio
of
about
53:1.
This
ratio
does
not
take
into
account
such
additional
costs as
those
for
managing
severe
toxic
cases,
for
medical
follow-
up
care
and
treatment,
remedial
education,
reduced
lifetime
earnings,
reduced
tax
payments,
or
reduced
earnings.
Over-
all,
monetized
costs
of
the
sequelae
in
lead
toxicity
cases-
are
spelled
out
by
U.S.
EPA
(24,37).
In
March
1987,
the
Committee
on
Environmental
Hazards,
American
Academy
of
Pediatrics
(47),
issued
a
statement
on
childhood
lead
poisoning,
including
a
recommendation
that
all
children
in
the
United
States
at
risk
of
exposure
to
lead
be
screened
for
lead
absorption
at
approximately
12
months
of
age
with
follow-up
testing
of
children
judged
to
be
at
high
risk
for
lead
exposure.
Currently,
the
Lead
Contamination
Control
Act
of
1988
(36),
described
earlier,
contains
provisions
which
call
for
the
U.S.
CDC
to
resume
oversight
and
support
of
U.S.
lead
screening
programs.
The
success
of
this
legislative
initiative
will
hinge
on
the
actual
level
of
funding.
Environmental
Hazard
Identification
and
Abate-
ment
for
Severe
Poisoning
Cases.
HAZARD
IDENTIFI-
CATION.
When
cases
of
toxicity
were
identified,
mass
screening
programs
for
lead
poisoning
routinely
made
efforts
to
identify
the
sources
of
exposure
as
part
of
secondary
prevention.
In
high-risk
populations
in
urban
areas,
leaded
paint
was
most
commonly
identified
as
the
likely
source
of
exposure
via
ingestion
(20-22).
However,
other
sources
were
implicated
in
other
cases,
since
a
significant
number
of
toxicity
cases
were
not
identified
with
leaded
paint.
LEAD
ABATEMENT
METHODS.
As
noted
earlier,
source-
specific
lead
abatement
actions
as
part
of
primary
exposure
prevention
have
had
mixed
success.
For
secondary
preven-
tion
methods,
the
principal
lead
source
at
issue
is
leaded
paint.
A
careful
examination
of
the
information
on
reducing
lead
exposure
by
completely
or
partially
removing
leaded
paint
clearly
shows
that
conventional
methods
often
result
in
incomplete
removal
and
often
carry
associated
exposure
risks.
In
a
prospective
study,
Chisolm
et
al.
(48)
observed
that
when
lead-poisoned
children
are
returned
to
"lead
abated"
structures,
their
PbB
levels
invariably
increase
to
unaccept-
able
levels.
This
does
not
appear
to
be
a
case
of
PbB
increase
from
the
endogenous
release
of
bone
lead,
since
children
similarly
exposed
before
treatment
do
not
have
such
PbB
elevations
when
placed
in
lead-paint-free
housing.
Information
has
accumulated
to
show
that
leaded
paint
removal
is
hazardous
to
the
workers
doing
the
removal,
and
lead
continues
to
be
hazardous
to
occupants
because
132
REDUCING
CHILDHOOD
LEAD
EXPOSURE
residual
material
has
been
removed
to
other
areas
accessible
to
young
children.
A
major
difficulty
is
the
relatively
high
mobility
of
old,
powdering
(chalking)
lead
paint,
which
enters
cracks
and
crevices,
settles
on
contact
surfaces,
and
readily
sticks
to
children's
hands.
As
Charney
et
al.
(26)
noted,
abatement
response
to
the
paint
dust
problem
may
well
be
as
important
as
removing
the
paint
film.
The
problem
of
continued
exposure
risk,
either
during
or
after
leaded
paint
abatement,
can
be
illustrated
in
the
recent
study
by
Rey-Alvarez
and
Menke-Hargrove
(49).
Rey-Alvarez
and
Menke-Hargrove
examined
lead-poisoned
children
(n
=
13)
whose
exposure
had
been
exacerbated
in
varying
ways
when
leaded
paint
was
being
or
had
been
removed.
Elevated
PbB
levels
were
further
increased
when
paint
was
removed.
Farfel
and
Chisolm
(50)
also
document
that
traditional
paint
removal
increases
household
dust
and
child
PbB
levels.
These
data
augment
the
experiences
of
other
investigators
and
make
it
clear
that
additional
lead
exposure
during
and
after
paint
lead
removal
can
occur.
Chisolm
(51)
has
drawn
attention
to
the
need
for
some
new
approaches
to
the
problem
of
removing
lead
from
occu-
pied
housing.
As
noted
earlier,
the
U.S.
HUD
is
examining
the
relative
effectiveness
of
paint
lead
removal
strategies
in
its
abatement
demonstration
program.
The
above
discussion
deals
with
the
elements
of
an
ideally
thorough
lead
removal
approach
as
part
of
general
risk
assessment
for
paint
lead.
The
extent
to
which
even
par-
tial
leaded
paint
abatement
will
lower
PbB
levels
overall
and
would
also
be
of
value
is
an
important
matter
but
is
more
an
issue
for
risk
management
(26).
A
hidden
assumption
underlies
efforts
to
remove
leaded
paint
from
the
homes
of
children
found
to
have
lead
poison-
ing:
that
the
child
will
remain
in
the
lead-abated
home.
In
reality,
there
is
high
residential
mobility
among
poor,
inner-
city
residents.
The
long-term
effectiveness
of
unsystematic
"spot"
abatement
is
questionable,
perhaps
even
for
the
individual
children
for
whom
the
effort
has
been
made.
Environmental/Biological
Prevention
Measures
This
approach
is
analogous
to
that
of
primary
preven-
tion
which
combines
nutrition
and
environmental
control.
Nutrition-based
measures
in
the
case
of
secondary
expo-
sure,
however,
might
be
more
problematic.
Specifically,
one
would
be
dealing
here
with
children
already
showing
signs
of
lead
toxicity.
A
secondary
nutritional
approach
would
also
require
that
the
affected
farnily
take
a
more
active
role
in
exposure
prevention,
and
this
raises
the
issues
of
com-
pliance,
family
budgets
for
adequate
diets,
etc.
Extra-Environmental
Prevention
Measures
These
measures
essentially
consist
of
legal
sanctions
to
force
the
removal
of
lead
from
residences
with
documented
poisoning
cases.
Such
sanctions
can
be
useful
tools
for
responding
to
demonstrated
and
significant
health
risks.
How
effectively
can
one
use
a
legal
framework
to
expedite
the
rapid
and
safe
removal
of
lead
hazards
from
children's
daily
environment?
Conversely,
can
one
conclude
from
avail-
able
information
that
a
real
handicap
for
such
action
is
the
absence
of
supporting
legal
tools?
Answers
to
these
questions
in
the
available
information
are
not
easily
found,
but
it
is
useful
to
examine
a
typical
major
screening
program
with
a
legal
component
and
assess
its
contribution
to
overall
abatement.
In
its
summary
of
screening
activities
submitted
to
ATSDR
(1),
the
City
of
St.
Louis
summarized
its
legal
actions
involving
landlords
and
others
who
own
housing
or
public-use
facilities
where
lead
poisoning
had
been
found.
A
summary
of
1985
court
activity
for
leaded
paint
ordinance
violations
indicated
a
case
load
of
1,086,
with
387
of
the
cases
carried
over
from
1984.
From
this
cumulative
docket,
154
defendants
were
fined
$2,447,
an
average
of
$16.
Minor
fines
appeared
to
be
the
only
measure
at
the
city's
disposal.
The
1984
count
was
virtually
identical
to that
of
1985,
and
the
average
fine
for
1984
was
the
same
as
for
1985.
One
cannot
say
whether
minor
fines
as
legal
sanctions
influenced
the
city's
lead
toxicity
rate
as
identified
from
screening.
In
the
most
recent
data,
this
rate
was
11%-a
rate
that
has
remained
about
the
same
since
1978,
owing
to
a
number
of
factors.
This
case
study
does
suggest,
how-
ever,
that
a
persisting
high
lead
toxicity
rate
has
not
led
to
more
effective
legal
measures.
Summary
and
Conclusions
Both
primary
and
secondary
lead
abatement
methods
have
been
examined
in
detail
in
this
article
and
the
report
to
Congress
(1)
which
gave
rise
to
it.
Certain
primary
lead
exposure
prevention
measures,
i.e.,
the
phasedown
of
lead
in
gasoline,
the
promulgation
of
ambient
air
lead
standards
for
stationary
source
emissions,
and
phase-out
of
lead-
soldered
food
cans
have
been
effective
in
reducing
overall
childhood
lead
exposure.
By
contrast,
other
lead
sources
and
pathways,
i.e.,
leaded
paint
in
older
U.S.
housing
and
public
buildings
and
lead
in
dusts
and
soils,
remain
as
significant
contributors
to
U.S.
childhood
lead
exposure
and
intoxication.
To
date,
little
in
the
way
of
nationwide
abatement
efforts
have
been
imple-
mented
for
these
routes
and
those
that
have
been
attempted
have
generally
failed.
Finally,
lead-contaminated
drinking
water
in
homes,
schools,
day-care
centers,
and
elsewhere
is
currently
a
sig-
nificant
source
of
exposure
for
pregnant
women
and
pre-
school
children.
While
there
are
proposed
or
newly
man-
dated
tapwater
lead
control
measures,
it
will
take
time
to
evaluate
their
relative
effectiveness.
As
might
be
expected,
the
relative
effectiveness
of
source-
specific
abatement
actions
in
the
United
States
has
been
closely
linked
to
their
implementation
through
centralized
control
strategies.
Such
measures
using
a
centralized
mech-
anism
are
typified
by
leaded
gasoline
phasedown,
ambient
air
lead
reduction,
and
regulation
of
lead
in
food
sources.
Lead
exposure
routes
that
are
widely
dispersed
through-
out
environmental
compartments
and
that
have
impacts
on
diverse
risk
populations
are
inherently
more
difficult
and
costly
to
control.
Such
difficulties
are
manifested
in
a)
the
high
levels
of
lead
in
the
paint
of
over
21
million
old
housing
133
134
MUSHAK
AND
CROCETTI
units
and
public
facilities;
b)
lead-contaminated
dusts
and
soils
in
urban
areas
and
other
sites
affected
by
airborne
and
other
lead
deposition;
and
c)
the
millions
of
U.S.
residential
units
and
public
facilities
having
contaminated
tapwater
due
to
lead-
soldered
plumbing,
lead
water
line
connectors,
and
lead-
containing
faucets
or
other
fixtures.
An
added
problem
in
the
case
of
either
leaded
paint
or
lead-contaminated
dusts
and
soils
is
the
extent
to
which
meaningful
lead
reduction
or
complete
removal
can
be
achieved.
This
arises
from
the
pervasive
distribution
of
the
contaminant
within
a
dwelling
unit
or
larger
area,
as
well
as
the
propensity
for
lead
to
be
highly
mobile.
For
exam-
ple,
it
is
quite
difficult
to
maintain
freedom
from
lead
con-
tamination
at
an
abated
site
if
neighboring
sources
provide
recontamination
by
leaded
paint
weathering
from
exterior
surfaces
(29-32)
or
leaded
dust
reentrainment/redeposition,
for
example.
Given
the
limitations
of
piecemeal
lead
abatement
actions,
exposure
reduction
approaches
are
needed
which
are
com-
prehensive
and
applicable
on
a
neighborhood
or
other
tract
basis.
This
is
not
to
say
that
individual
sites
of
exposure,
associated
with
identified
lead
intoxication,
would
not
benefit
from
abatement
efforts.
The
relative
value
of
secondary
versus
primary
exposure
prevention
methods
is
markedly
affected
by
trends
in
the
human
toxicology
and
environmen-
tal
epidemiology
associated
with
lead
exposure.
As
the
levels
of
lead
exposure
and
associated
levels
of
lead
body
burden,
i.e.,
PbB
considered
safe,
continue
to
be
adjusted
downward
(22,47),
it
is
increasingly
clear
that
primary
exposure
control,
rather
than
secondary
methods
such
as
screening
plus
medical
intervention,
will
be
the
prin-
cipal
regulatory
option.
For
example,
PbB
levels
below
25
Atg/dL
are
still
of
significant
public
health
concern
and
are
typical
of
exposure
for
millions
of
children
and
other
risk
subjects,
but
it
is
neither
medically
appropriate
nor
feasible
to
employ
chelation
therapy
and
other
medical
treatments
in
response
to
such
body
lead
burdens.
The
only
solution
is
reduction
or
removal
of
the
sources
of
lead
exposure.
The
authors
thank
Barry
L.
Johnson,
Associate
Administrator,
ATSDR
and
Agency
coordinator
for
the
report
to
Congress,
for
his
support.
We
also
gratefully
acknowledge
the
logistical
and
technical
inputs
of
Lester
D.
Grant
and
J.
Michael
Davis,
Environmental
Criteria
and
Assessment
Office
(ECAO),
U.S.
Environmental
Protection
Agency.
We
also
thank
the
many
governmental
and
nongovernmental
lead
experts
who
provid-
ed
critical
peer
review
of
the
various
drafts
of
the
Congressional
report.
Finally,
we
thank
Vandy
Bradow,
ECAO/EPA,
for
seeing
to
the
pro-
duction
of
the
Congressional
report
and
especially
Miriam
Gattis
and
Lorrie
Godley
for
their
support
staff
assistance.
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July
1988
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Toxic Substances
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