Editorials
References
1.
Loughlin
AM,
Marchant
CD,
Lett
SM.
The
changing
epidemiology
of
invasive
bacterial
infections
in
Massachusetts
chil-
dren,
1984
through
1991.
Am
J
Public
Health.
1995;85:392-394.
2.
Centers
for
Disease Control
and
Preven-
tion.
Progress
toward
the
elimination
of
Haemophilus
influenzae
type
b
disease
among
infants
and
children-United
States,
1987-1993.
MMWR.
1994;43:144-148.
3.
Centers
for
Disease
Control.
Retrospective
assessment
of
vaccination
coverage
among
school-aged
children-selected
U.S.
cities,
1991.
MMWR.
1992;41:10(3-107.
4.
Zell
ER,
Dietz
V,
Stevenson
J,
et
al.
Low
vaccination
levels
of
US
preschool
and
school-age
children.
Retrospective
assess-
ments
of
vaccination
coverage,
1991-1992.
JAMA.
1994;271:833-839.
5.
Centers
for
Disease
Control
and
Preven-
tion.
Vaccination
coverage
surveys
in
county
health
departments-Kansas,
1993-1994.
MMWR.
1995;44:244-247.
6.
Davis
SF,
Strebel
PM,
Atkinson
WL,
et
al.
Reporting
efficiency
during
a
measles
outbreak
in
New
York
City,
1991.
Am
J
Public
Health.
1993;83:1011-1015.
7.
Centers
for
Disease Control
and
Preven-
tion.
Resurgence
of
pertussis-United
States,
1993.
MMWR.
1993;42:952-960.
8.
Simpson
KN,
Biddle
AK,
Rabinovich
NR.
A
model
for
estimating
the
impact
of
changes
in
children's
vaccines.
Am
J
Public
Health.
1995;85:1666-1672.
9.
Fairbrother
G,
DuMont
KA.
New
York
City's
1993
Child
Immunization
Day:
plan-
ning,
costs,
and
results.
Am
J
Public
Health.
1995;85:
1662-1665.
10.
Robinson
CA,
Evans
WB,
Mahanes
JA,
et
al.
Progress
on
the
childhood
immuniza-
tion
initiative.
Public
Health
Rep.
1994;109:
594-600.
11.
Hueston
WJ,
Mainous
AG
III,
Farrell
JB.
Childhood
immunization
availability
in
primary
care
practices.
Effects
of
programs
providing
free
vaccines
to
physicians.
Arch
Fam
Med.
1994;3:605-609.
12.
Joint
WHO/UNICEF
Statement.
Plan-
ning
principles
for
accelerated
immuniza-
tion
activities.Assignment
Children.
1985;69/
72:
139-154.
13.
Szilagyi
PG,
Rodewald
LE,
Humiston
SG,
et
al.
Immunization
practices
of
pediatri-
cians
and
family
physicians
in
the
United
States.
Pediatr.
1994;94:517-523.
14.
Ruch-Ross
HS,
O'Connor
KG.
Immuniza-
tion
referral
practices
of
pediatricians
in
the
United
States.
Pediatr.
1994;94:508-
513.
15.
Bernier
RH.
Toward
a
more
population-
based
approach
to
immunization:
fostering
private
and
public-sector
collaboration.
Am
J
Public
Health.
1994;84:1567-1568.
Editorial:
Research
on
the
Effects
of
Prenatal
Alcohol
Exposure-A
New
Direction
Since
the
first
reports
of
birth
defects
among
offspring
of
alcoholic
women,
the
field
of
fetal
alcohol
research
has
made
considerable
advances
in
defining
the
impact
and
the
long-term
consequences
of
heavy
drinking
or
alcoholism
during
pregnancy.
A
definition
of
fetal
alcohol
syndrome
arrived
at
by
consensus
has
advanced
the
comparability
of
research
and
clinical
data
across
sites.
The
diagno-
sis
requires
effects
in
three
different
domains:
morphological
anomalies,
spe-
cifically
facial
anomalies;
growth
retarda-
tion;
and
deficits
in
the
development
of
the
central
nervous
system.
'
Furthermore,
we
have
defined
a
series
of
"fetal
alcohol
effects"
or
"alcohol-related
birth
defects"
that
do
not
meet
the
syndrome's
criteria
but
that
can
be
correlated
statistically
with
alcohol
use
during
pregnancy.
Research
on
fetal
alcohol
syndrome
is
by
no
means
exhausted.
However,
we
have
made
considerable
strides
in
under-
standing
some
of
the
consequences,
if
not
the
mechanism,
of
heavy
drinking
and
alcoholism
during
pregnancy.
As
a
result,
an
argument
can
now
be
made
for
focusing
on
a
different
question:
the
short-
and
long-term
effects
of
lower
levels
of
drinking.
Although
children
of
drinking
mothers
can
be
affected
in
the
absence
of
the
full-blown
syndrome,
little
is
known
about
the
magnitude,
timing,
dose,
or
pattern
of
exposure
that
might
bring
about
the
sequelae.
The
public
health
message
about
the
consequences
of
drinking
during
preg-
nancy
has
been
effective.
National
data
from
the
mid
1980s
show
that
drinking
during
pregnancy
decreased
over
that
period.2
In
our
own
study,
women
often
tell
us
that
they
have
decreased
their
drinking
to
protect
their
babies.
However,
women
still
do
drink
during
pregnancy.
In
a
national
sample,
25%
of
women
re-
ported
drinking
during
pregnancy2;
among
lower
income
women
in
our
study,
substan-
tially
more
drank.3
In
both
studies,
the
majority
of
drinkers
were
not
drinking
heavily,
and
of
those,
the
majority
who
drank
did
so
early
in
pregnancy,
decreas-
ing
their
use
by
the
end
of
the
first
trimester.
We
have
little
information
on
the
outcomes
of
the
pregnancies
of
women
who
drink
at
these
lower
levels,
even
though
they
represent
the
majority
of
the
drinking
population
during
pregnancy.
Reports
from
our
studies3.4
and
oth-
ers56
have
shown
that
alcohol
use,
even
at
levels
of
less
than
a
drink
per
day,
can
affect
growth
and
development.
In
this
issue
of
the
Journal,
Larroque
et
al.
report
that
they
detected
effects
on
the
develop-
ment
of
the
fetus's
central
nervous
system
at
maternal
intake
levels
of
three
or
more
drinks
per
day.7
In
each
of
these
studies,
the
effects
are
small
and
would
not
be
considered
clinically
significant.
It
would
be
a
mistake,
however,
to
discard
them
as
unimportant.
Although
small,
they
serve
as
a
marker
of
the
effects
of
a
teratogen
and
as
a
sign
that
the
growth
and
achievement
of
these
exposed
individuals
might
be
less
than
they
could
have
been.
Moreover,
these
measurable
effects
may
reflect
other
problems
that
we
have
yet
to
investigate
or
even
see.
Another
reason
for
studying
lower
levels
of
maternal
drinking
is
to
determine
the
shape
of
the
alcohol-fetal
relation-
ship.
Our
data
indicate
that
prenatal
alcohol
exposure
has
a
dose-response
or
linear
effect
on
growth.3
Animal8
and
human9
data
indicate
that
alcohol's
effect
on
the
central
nervous
system
may
be
best
modeled
as
a
threshold
rather
than
a
dose-response
effect.
These
findings
have
major
implications
for
our
understanding
of
drinking
during
pregnancy
and
for
our
ability
to
educate
and
counsel
women
on
the
consequences.
If
there
is
a
threshold,
then
conceivably
there
is
a
safe
level
of
drinking.
If
the
relationship
is
a
dose-
response
one,
then
there
is
no
safe
level
of
exposure.
Probably,
alcohol
will
affect
systems
differently,
in
some
cases
as
a
dose-response
and
in
others
as
a
thresh-
old
relationship.
To
date,
there
has
been
little
investigation
of
this
issue,
although
investigators
have
used
implicit
threshold
models
by
analyzing
their
data
categori-
cally,
and
explicit
dose-response
models
by
using
regression
analyses.
Heavy
drinking
and
alcoholism
lead
to
fetal
exposure
levels
and
effects
so
global
that
the
basic
science
of
teratology
is
difficult
to
apply.
In
the
teratologic
model,'0
the
size
of
the
effect
increases
Editor's
Note.
See
related
article
by
Larroque
et
al.
(p
1654)
in
this
issue.
1614
American
Journal
of
Public
Health
December
1995,
Vol.
85,
No.
12
Editorials
with
the
dose
within
a
given
domain
of
effects.
Thus,
as
the
exposure
increases,
the
growth
deficit
also
increases.
A
second
premise
of
the
model
is
that
the
number
of
affected
systems
increases
with
the
dose.
Offspring
prenatally
exposed
to
large
amounts
of
alcohol
will
be
affected
across
more
domains
(e.g.,
central
ner-
vous
system,
growth,
and
morphology)
than
offspring
exposed
to
lower
levels.
Studying
lower
levels
of
exposure
allows
us
to
study
more
subtle
effects
and
to
separate
the
effects
and
the
order
of
the
effects
of
dose.
The
teratologic
model
further
posits
that
the
effects
of
exposure
will
vary
depending
on
the
time
of
exposure
during
pregnancy.
It
is
not
possible
to
isolate
timed
effects
among
the
offspring
of
women
who
drink
heavily
and
throughout
pregnancy.
However,
it
is
possible
to
study
women
who
change
their
drinking
pat-
terns
and
to
begin
to
formulate
hypoth-
eses
about
which
points
in
fetal
develop-
ment
are
susceptible
to
alcohol
exposure.
Timing
is
important
for
prognostic
rea-
sons.
For
example,
growth
deficits,related
to
first-trimester
exposure
tend
to
be
symmetrical,
with
the
children
not
exhibit-
ing
catch-up
growth,
whereas
growth
deficits
associated
with
exposure
later
in
pregnancy
tend
to
be
asymmetrical,
and
the
exposed
children
usually
catch
up
to
the
growth
patterns
of
nonexposed
chil-
dren
after
birth.1",2
Thus,
understanding
the
role
of
timing
in
how
alcohol
exposure
affects
growth
has
long-term
implications.
Carefully
designed
studies,
analytic
models,
and
measurement
tools
are
neces-
sary
in
the
study
of
lower
levels
of
maternal
drinking.
A
primary
concern
is
the
measurement
of
alcohol
use
during
pregnancy.
This
is
at
best
a
difficult
task,
given
that
drinking
varies
in
quantity,
frequency,
beverage
type,
size
of
drink,
and
duration
of
drinking
episodes,
to
name
just
a
few
of
the
variables.
Further-
more,
it
is
essential
to
know
how
these
patterns
coincide
with
the
timing
of
fetal
development.
We
need
to
develop
meth-
ods
for
precise
intake
measurement
as
well
as
to
apply
new
tools
for
both
assessment
and
analysis.
Simple
recourse
to
biological
measures
does
not
answer
this
dilemma,
since
they
do
not
describe
drinking
patterns,
dose
per
episode,
and
other
important
factors
that
determine
the
effects
of a
teratogen.
We
estimate
these
relationships
by
analyzing
the
ef-
fects
of
exposure
during
different
and
defined
periods
of
pregnancy,
by
assessing
the
effects
of
drinking
changes
during
pregnancy,
and
by
differentiating
the
effects
of
patterns
such
as
binge
and
continuous
drinking.
Another
issue
that
must
be
ad-
dressed
is
the
measurement
of
the
covari-
ates
of
alcohol
use.
Women
who
drink
during
pregnancy,
and
particularly
those
who
continue
to
drink
throughout
preg-
nancy,
are
more
likely
to
use
other
substances
and
have
less
prenatal
care,
poorer
maternal
health,
and
lower
socio-
economic
status.13
Each
of
these
factors
is
in
itself
a
risk
factor
for
poor
pregnancy
outcome.
These
factors
must
be
measured
with
the
same
level
of
care
as
alcohol
use
if
we
are
to
separate
the
effects
of
prenatal
exposure
to
alcohol
from
those
of
factors
that
accompany
alcohol
use.
Thus,
the
time
has
come
to
explore
the
effects
of
alcohol
exposure
during
different
stages
of
pregnancy,
the
effects
of
differing
patterns
of
alcohol
use
during
pregnancy,
and
the
shape
of
the
relation-
ships
between
exposure
and
outcomes.
With
this
knowledge,
we
can
begin
to
clarify
the
mechanisms
of
alcohol's
effects
during
pregnancy.
This
research
requires
that
we
look
at
the
full
spectrum
of
drinking
behavior,
rather
than
focusing
on
the
most
exposed
or
the
alcoholic
preg-
nancy.
These
studies
have
the
potential
to
contribute
to
the
basic
science
of
the
field.
In
addition,
this
research
will
provide
women
with
accurate
information
about
the
consequences
of
prenatal
drinking
and
the
long-term
effects
of
prenatal
alcohol
exposure
on
their
children.
C]
Nancy
L.
Day
Western
Psychiatric
Institute
and
Clinic
University
of
Pittsburgh
School
of
Medicine
References
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R,
Clarren
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of
prena-
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Res.
1989;13:597-598.
2.
Serdula
M,
Williamson
D,
Kendrick
J,
Anda
RF,
Byers
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Trends
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by
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3.
Day
N,
Jasperse
D,
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G,
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on
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and
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1989;84:536-541.
4.
Day
N,
Richardson
G,
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D,
Robles
N.
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marijuana
and
tobacco:
the
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on
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and
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at
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1994;18:786-794.
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Jacobson
J,
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S.
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and
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where
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Alcohol
Health
World
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6.
Shu
X,
Hatch
M,
Mills
J,
Clemens
J,
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M.
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alcohol
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caffeine
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and
fetal
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Kaminski
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Dehaene
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M,
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D.
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December
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Vol.
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No.
12
American
Journal
of
Public
Health
1615
