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CHAPTER 2
Etiology and Risk Factors
Despite important new research findings and improvements in the
science of obstetr ics, our understanding of the basic causes of preterm
labor and intrauterine growth retardation Is 1 imited . In the absence
of adequate knowledge about etiology, a large body of information has
developed about factors associated with low birthweight, often termed
frisk factors, n because their
an increased chance, or risk, of bearing a low b~rthweight infant.
This chapter outlines data both on the etiology of prematurity and IUGR
and on the risk factors associated with these outcomes of pregnancy.
It also describes the process of risk assessment and analyzes several
risk assessment systems.
presence in an individual woman indicates
Etiology
As described in the previous chapter, the term low birthweight can
refer to three often intertwined outcomes of pregnancy: preterm
delivery, intrauterine fetal growth retardation (TUGR), and a
combination of both. Although little is known about the various
mechanisms that produce these conditions, several
have been developed as a basis for further
this section.
~ .
Prematurity
theoretical models
research and are outlined in
The mechanism for the initiation and maintenance of normal human
labor is not known, but substantial progress has been made in
understanding some of the important associated physiologic and
biochemical events. ~ Information about the onset of preterm labor is
more fragmentary and speculative. 2
Endocrine changes in the uteroplacental environment appear to be
the principal factors leading to the development of uter ine
contractions. 3 These endocrine changes involve hormones from both
the mother and the fetus; cor tisol, estrogen, and progesterone appear
to play ma jor roles . Much of this informal ion is based on stud ies o f
sheep in which the process starts about 10 days before labor.
46
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47
The first event in sheep Is an elevation in fetal cortisol,
probably in response to fetal ACTH. This cortisol rise generates a
decline in maternal progesterone due to the induction of 17
a-hydroxylase enzyme activity in the placenta, which increases the
conversion of progesterone to dehydroxyprogesterone. 4 Progesterone
withdrawal is associated with increased uterine muscle excitability, or
responsiveness to electrical and hormonal stimuli. Dehydroxyproges-
terone also is a precursor of the rise in maternal estrogen, which
occurs a few days before the onset of labor. Estrogens increase
rhythmic uterine contractions and also the responsiveness of the uterus
to oxytocin e In sheep, estrogen elevation also causes a rise in
prostagland~n (PGF2a) production hours before the onset of uterine
activity. The combined changes in maternal hormones are thought to
affect uterine muscle by enhancing myometrial excitability and the
conduction of action potential.
In contrast to sheep, the human hormonal changes appear to occur
during the last 5 weeks of pregnancy, and evidence for fetal cortisol
initiating the onset of labor is lacking. Amniotic fluid cortisol and
maternal blood estrogen increase at 34 to 36 weeks of gestation. The
former correlates with fetal pulmonary maturity and the latter may play
a role by increasing prostaglandin production. Unlike in sheep, the
role of progesterone in human labor is unclear .3 A decline In
peripheral blood levels before labor has been suggested in at least one
study, 5 although others have failed to confirm this finding. The
presence of a fetal membrane progesterone binding protein, possibly
facilitated by estrogen, indicates that a local withdrawal effect may
occur. Several reports indicate that prostaglandins do play a role in
human labor; they are synthesized from a fatty acid precursor In the
chorioamnion and/or decidua at a time when estrogen levels are
increasing.6 7 Last, increased levels of maternal oxytocin are not
thought to contribute to initiating labor (although a threshold level
may be important as a permissive factor), but may be necessary for the
development of more intense contractions during the second stage of
labor. Fetal oxytocin may play a role, however, as indicated by high
concentrations of this hormone in umbilical cord blood.
The way in which hormonal changes act to induce labor Is not
clear .2 3 Animal studies demonstrate that low resistance myometria1
pathways (gap junctions) form dur ing labor and suggest that the
structural and biochemical organization of myometrial muscle may be
important in the development of contractions. The development of gap
junctions under the influence of steroids and prostagland~ns and in
relation to the estrogen/progesterone ratio is probably of major
importance to the organization of the myometrium.8 The contraction
of uterine muscle is significantly influenced by an increase in the
concentration of free calcium on the myofibrils resulting from the
action of prostaglandins, which counteracts progesterone-~nduced
calcium binding In the sarcoplasm~c reticulum.
Knowledge about the etiology, initiation, and maintenance of
preterm labor is limited. 2 9 A The underlying pathophysiology is
postulated on the basis of variations from the normal patterns of
hormonal effects detected in animals and man or on the basis of
-
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48
inferences made about the possible untoward effects of certain clinical
conditions on uteroplacental physiology. Observations suggest that
infection, stress, hypertension, and other conditions may be associated
with variations in the endocrine environment and metabolic state of the
uterus and the cervix. These variations probably result from complex
interactions involving progesterone, estrogen, oxytoc in, and other
hormones; prostaglandins; calcium ions; adrenergic agents and
receptors; catecholamines; and~uteroplacental blood flow.
From the foregoing, it is clear that at this time it is not
possible to identify a single etiology for premature birth.2 It is
possible, however, to enumerate a variety of factors and clinical
conditions that have been associated with the preterm onset of labor.
This list includes, but is not limited to, abruptio placentae,
amnionitis, congenital malformations, erythroblastosis fetalis,
incompetent cervix, placenta previa, polyhydramnios, preeclampsia,
premature rupture of membranes, severe maternal illness, multiple
pregnancies, and urinary tract infections. In general, these are
conditions in which there is an inability of the uterus to retain the
fetus, interference with the course of the pregnancy, premature
separation of the placenta, or a stimulus to effective uterine
contractions before term. Several of these conditions are discussed
later in the chapter as risk factors for preterm birth, although it is
apparent that the distinction between a r isk factor and a causal
mechanism is not always clear. Finally, in many cases of premature
birth, no association with a pathologic factor can be identified.
_
Intrauterine Growth Retardation (IUGR)
Delay in the growth and development of the fetus has been
associated with a variety of factors that can be grouped in terms of
the locus of their impact: the placenta, the pregnant woman herself,
the fetus, or some combination of these. In general, IUGR is
associated with conditions that interfere with the circulation to and
efficiency of the placenta, with the development or growth of the
fetus, or with the general health and nutrition of the pregnant woman;
however, for many growth-retarded infants no relevant pathogenic
factors can be identified.
Vascular and inf lammatory lesions of the placenta; placental
separation and infarction; and decreases in placental weight,
cellularity, and surface area may act alone or in combination to
produce TUGR.~ It is postulated that such conditions result
directly or indirectly in a reduction in the supply of nutrients to the
fetus. 12 Multiple pregnancies (for example, twins or triplets) also
may be associated with IUGR because the placenta may be unable to
supply sufficient nutrients to multiple fetuses. Other placental
conditions associated with IUGR include hemangioma of the placenta or
umbilical cord and the parabiotic transfusion syndrome. Insufficient
placental transfer of nutrients may be primarily related to abnormal
transport across the placenta, to alterations in placental metabolism,
or to changes in the uteroplacental circulation. 3
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49
Certain conditions or diseases of pregnant women also are
associated with IUGRe ~ 4 ~ 5 They are thought to directly or
indirectly hamper delivery of nutrients or oxygen to the uteroplacental
circulation, which results in an inability to maintain normal fetal
growth and development. 6 The most frequent, recognized problem Is
the presence of a maternal vascular disease, such as chronic hyper-
tension or chronic renal disease. The duration and severity of the
~ . . ~ . . . ~
absorber are roughly refaced co One severity of the IUGR. Pregnancy-
induced hypertension also can cause IUGR, but commonly the fetus is
delivered before severe growth retardation develops. This condition,
super imposed on chronic hypertension, often is associated either with
IUGB or premature delivery of a fetus that has grown and developed
normally up to the time of delivery. Severe forms of diabetes mellitus
_ . . . ~ · . ,
also are frequently associated with vascular disease and IOGR. Sickle-
cell disease may be associated with IUGR and placental lesions.
Several conditions that lead to hypoxia in pregnant women have been
associated with IUGR, including cyanotic heart or pulmonary disease and
residence at high altitudes. 6 ~ 7 A variety of mechanisms have been
postulated for the development of IUGR associated with cigarette
smoking, alcohol and narcotic ingestion, and the administration of
antimetabolites, but no definitive statement can be made concerning
these etiologies. Similarly, the precise pathogenic mechanisms linking
maternal malnutr ition and chronic illness during pregnancy to low
birthweight (IUGR or prematurity) are unknown.
Fetal factors implicated by association in the etiology of IUGR
include chromosomal disorders, such as certain autosomal trisom~es;
chronic fetal infections, such as congenital rubella, syphilis, and
cytomegalovirus inclusion disease; certain congenital malformations and
diseases; and radiation injury. ~8 Although a variety of
pathogenic mechanisms have been suggested by these associations, the
specific etiologies have not been established conclusively.~5
Finally, TUGR and prematurity occur together in about 30 percent of
low birthweight cases. In some instances, both the prematur ity and the
IUGR occur without a demonstrable association with a suspected
pathogenic factor. In other cases, various combinations of the factors
discussed above can be identified.
Risk Factors: An Overview
Recent research on the risk factors associated both with preterm
delivery and TUGR has helped to identify possible causes of low
b~rthwe~ght. Risk factor analysis also helps guide clinical practice
and suggests possible prevention strategies at both the individual and
population level.
Unfortunately, the risk factor literature has many methodological
and conceptual problems that make its interpretation cliff icult. For
example, many studies analyze the relationship of a given risk factor
to slow birthweight" rather than to the more specific outcomes of
preterm delivery and intrauterine growth retardation; also, these
studies commonly rely on estimates of gestational age, which often are
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so
approximate. Risk factors often are defined differently in different
studies, and studies of small groups often do not produce information
that can be applied to other populations, thereby hampering comparisons
and pooling of data. More importantly, many studies examine risk
factors as independent entities, although several factors may cluster
in an individual and may be causally related. Finally, known confound-
ing variables may not be controlled, and the cross-sectional design of
many r isk factor studies makes it cliff icult to separate cause and
effect. Such problems make it hard to reach conclusions about the
magnitude of risk posed by single factors.
Some of these limitations can be overcome by more careful statis-
tical design and definition. Others are more difficult to correct.
For example, many population-based studies must rely on data derived
from birth certificates; in most states, these forms include only a
limited number of risk factor variables relevant to low birthweight.
Birth certificates in most states do not provide information on such
factors as maternal height, weight, weight gain during pregnancy, or
smok ing practices .
A chart listing the principal risk factors for low birthweight is
shown in Appendix A. Based on the studies noted in the appendix, in
this chapter, and in Chapter 3, the chart records whether a given
factor has been reported to increase the risk of preterm delivery or
IUGR, or whether it has simply been linked to low birthweight. For
some factor s, the char t also records attr ibutable and relative r isk
values (defined In Chapter 11. Appendix A includes a mixture of
factors for which the evidence of risk is strong and those for which
the association with prematurity and/or IUGR is less clear.
Because some studies have calculated relative or attributable risk
values for certain factors , the committee explored the possibility of
ranking the risks in order of magnitude to help set priorities for
interventions and for further research. Unfortunately, the data do not
permit such ordering. For some factors (including many of the
infections), the committee was able to locate no risk values at all
For many others, only a single value was located, and the committee
judged this to be an inadequate data base from which to construct a
ranking of magnitude of r isk . Another problem is that r isks imE,or ten t
at an individual level are not always so for populations. It is also
apparent that the estimates of risk vary significantly, probably due to
def initional var. Cations and to differences in populations studied. The
committee also concluded that, because of the numerous interrelation-
ships among factors, it would be unwise to address them in a way that
suggests each always has an independent influence on preterm delivery
or IUGR.
Even without an orderly ranking of risk, the committee found that
the factors could be grouped in a way that helps to structure
preventive interventions, which is the pr incipal focus of the repor t.
In Table 2.1, which summarizes Appendix A, the risk factors are
separated into demographic characteristics, medical risks that can be
detected before conception, risks that can be detected during
pregnancy, behavioral and environmental r isks, health care r isks, and a
final category of factors whose role in low birthweight is still being
def ined.
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51
TABLE 2.1 Principal Risk Factors for Low Birthweight
I. Demographic Risks
A. Age (less than 17; over 34)
B. Race (black)
C. Low socioeconomic status
D. Unmarried
E. Low level of education
II. Medical Risks Predating Pregnancy
A. Parity (D or more than 4)
B. Low weight for height
C. Genitourinary anomalies/surgery
O. Selected diseases such as
diabetes, chronic hypertension
E. Nonimmune status for selected
infections such as rubella
Poor obstetric history, including
previous low birthwe~ght infant,
multiple spontaneous abortions
Maternal genetic factors (such as
low maternal weight at
own birth)
III. Medical Risks in Current Pregnancy
A. Multiple pregnancy
B. Poor weight gain
C. Short interpregnancy interval
D. Hypotension
E. Hypertension/preeclampsia/toxemia
F. Selected infections such as
symptomatic bacteriuria, rubella,
and cytomegalovirus
G. First or second trimester bleeding
H. Placental problems such as
placenta previa, abruptio
placentae
I. Hyperemesis
J. Oligohydramnios/polyhydramnios
R. Anemia/abnormal hemoglobin
L. Iso~mmunization
M. Fetal anomalies
F.
G.
N. Incompetent cervix
0. Spontaneous premature rupture
of membranes
IV.
V.
Behavioral and Environmental Risks
A. Smoking
B. Poor nutritional status
C. Alcohol and other substance abuse
D. DES exposure and other toxic
exposures, including occupa-
tional hazards
E. High altitude
Health Care Risks
A. Absent or inadequate prenatal
care
B. Iatrogenic prematurity
VI. Evolving Concepts of Risk
A.
B.
C.
Stress, physical and psychosocial
Uterine irritability
Events triggering uterine
contractions
D. Cervical changes detected before
onset of labor
E. Selected infections such
mycoplasma and Chlamydia
trachomatis
F. Inadequate plasma volume
expansion
G. Progesterone deficiency
This grouping leads to the observation that many of the risk
factors for low birthweight (categories I, II, and IV of the table) can
be identified before pregnancy occurs; detection and possible
intervention need not always wait until the prenatal per iod . Chapter 5
develops this theme more fully. The grouping also helps to highlight
the importance of behavioral and environmental risks anu one neec~ tor
interventions that go beyond medical care. The demographic measures
can help to define target populations. The cluster of health care
issues highlights the fact that not all r isks for low birthweight
~ ~ .
_
-
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~2
derive from characteristics of women themselves. And finally, the
category of evolving concepts of risk suggests some important research
areas for improved understanding of low birthweight. These themes
appear throughout Part lI of this report.
In the following detailed discussion of risk factors, the committee
chose to focus on those that are widely distr ibuted throughout the
population, amenable to prevention or treatment, or especially
controversial. These include the demographic risk factors of race,
age, and socioeconomic status; the medical and obstetr ic r Asks of
hypertension/preeclampsia, diabetes, obstetric history (including
previous induced abortion), multiple pregnancy, and infection;
nutr ition; the behav ~ oral and environmental r isks of smok ing and
alcohol use; and iatrogenic prematur ity. The committee also examines
certain r isk factors that are more speculative in nature, including
stress, uterine irritability, cervical changes, inadequate plasma
volume expansion, and progesterone deficiency.
Chapter 3, a review of state and national vital statistics data,
provides additional information on some of the demographic factors and
on the issues of pregnancy interval, obstetr ic history, and parity in
relation to age. Chapter 6 explores another risk factor for low
birthweight, absent or inadequate prenatal care.
Demographic Risks
The interrelationships among the major demographic risk factors are
numerous and it is often difficult to determine the precise association
between any single factor and low birthweight . Nonetheless , through
careful statistical design, the independent effect of each is gradually
be ing def ined .
Race
Table 2.2 shows the frequency of low birthweight for different
racial and ethnic groups. The approximate 2:1 low birthweight ratio
between black and nonblack ethnic groups has remained fairly constant
for the past 20 years. When ~ ow birthweight infants are subdivided
into those born at term and those born prematurely, blacks remain
approximately twice as likely as whites to be in either category.~9
In one large but now dated study of approximately 50,000 pregnancies,
black newborns were on average 233 grams lighter than the' r white
counterparts .2 0
That black neonates are at high risk of low b~rthweight is
unquestioned. The reason or reasons for this r isk are uncertain,
however. Maternal age may account for part of the increased r isk.
Teenage mashers are at high risk of low b~rthweight, and black mother
are more likely to be teenagers than are mothers of other ethnic
groups. In 1980, 26.5 percent of all black births were to teenagers.
In contrast, 12.1 percent of white births and 15.3 percent of Hispani
births were to teenagers. When black and white mothers of the same
. s
ic
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53
TABLE 2.2 Percentage of Live Births Less Than 2,500 Grams
Percent Less
Than 2,500 Grams
Percent Less
Than 1,500 Grams
White 5~7a 0.9a
Black 12.5a 2.4a
Chinese 4.9a o.6a
Mexican-American S.3b o.9b
American Indian 6.9c --
SOURCES:
aNational Center for Health Statistics: Characteristics of Asian
Births: United States, 1980. Prepared by S Taffel. Monthly Vital
Statistics Report, Vol. 32, No. 10 (supplement). Public Health ~
Washington, D.C. : U.S. Government Printing Office, February 1984 .
National Center for Health Statistics: Births of Hispanic Parentage,
1979. Prepared by SJ Ventura. Monthly Vital Statistics Report, Vol.
31, No. 2 (supplement). Public Health Service. Washington, D.C.: U.S.
Government Printing Office, May 1982.
CNational Center for Health Statistics: Factors Associated with Low
Birthweight, 1976 . - ~ - ~ ~ ~ -- ~ ~ ~ - ~ ~ - ~ ~ ~
Series 21, No. 37.
Prepared by S Taftel. Vital and Health Statistics,
DHEW No. (PHS) 80-1915. Public Health Service.
Washington, D.C.: U.S. Government Printing Office, April 1980.
age are compared, however, blacks are at higher risk of low birthweight
in every age group.22 The relationship of low birthweight to maternal
age using 1976 data is shown in Table 2 .3; Appendix Table B.7 displays
more recent and more detailed data on the same subject.
Low level of maternal education is another r isk factor for low
birthweight and is often used as a proxy for socioeconomic status.
Table 2.4 shows the relationship between race, education, and low
birthweight. In general, black mothers are less educated than white
mothers. In 1980, 35 percent of black women who delivered live-born
babies had completed less than 12 years of school, versus 20 percent of
whites. At the other end of the educational spectrum, 16 percent of
white mothers and 6 percent of black mothers were college graduates.2i
Educational differences do not account for the racial differences in low
birthweight, however. When matched for both age and education, blacks
are still at higher risk of low birthweight.22 See also Appendix
Table B.9.
Black women are more likely than white women to delay initiation of
prenatal care.2 ~ However, when receipt of prenatal care is held
constant, black women are still at increased risk of delivering a low
birthweight baby.2 3 A limitation of most studies in this area is the
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54
TABLE 2.3 Maternal Age and Percentage of Infants Less Than 2,500
Grams, 1976
Maternal Age
(year s)
ite Black
{percent) (percent)
Less than 15 11.8 17 .1
15-19 8.1 14.7
20-24 6.0 12.6
25-29 . 5 .3 11.3
1
30-34 5.8 11.6
35-39 7.0 13.1
40-44 8.3 12.8
45 49 9.4 16.3
SOURCE: National Center for Health Statistics: Factors Associated with
Low Birthweight, 1976. Prepared by S Taffel. Vital and Health
Statistics, Series 21, No. 37. DHEW No. (PHS) 80-lgl5. Public Health
Service. Washington, D.C.: U.S. Government Printing Office, April 1980.
inability to adjust for the quality or content of prenatal care
received. Chapter 6 takes up this issue in detail.
To control for the effects of other variables that may be related
to race, such as maternal stature, smoking, and others that are not
included on birth certificates, one can look at special studies, such
as the Collaborative Perinatal Study, which, though dated, remains an
important and detailed survey of a number of important issues and
processes in pregnancy. At the time of that project, fewer black than
white women smoked, and among the smokers, white women smoked more than
black women. When smoking status was controlled, blacks were still
twice as likely as whites to have low birthweight infants. The height
distributions of blacks and whites were almost identical, while blacks
tended toward slightly higher prepregnant weights. At almost every
combination of height and weight, and for almost every combination of
weight and weight gain, black women were at hither risk of low
birthweight Than white women.
Furthermore, black women were at higher
risk of low birthweight at all combinations of age and parity.20
Finally, it has been shown that women whose last infant was of low
birthweight are at increased risk of low birthweight in the current
pregnancy.24 Yet in the Collaborative Study, when women were
stratified by whether or not their last child was low birthweight,
blacks were still at increased risk of low birthweight during the
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55
TABLE 2.4 Percentage of Single Live Births Less Than 2,500 Grams by
Race and Educational Attainment of Mother
White
Maternal Educational
Atta inment
(year s ~
1972 1977
(percent) (percent)
Black
1972 1977
(percent) (percent)
Less than 12 7 .29 6 .99 13 .59 13 .04
12 5.16 4.74 10.85 10.31
13-15 4.43 4 .09 9.76 9.41
16 or more 3.97 3.63 8.92 8.15
NOTE: Adjusted for maternal age and total birth order. Women under
age 20 excluded.
SOURCE: National Center for Health Statistics: Trends and variations in
birth weight. Prepared by JC Rleinman. In Bealth, United States, 1981,
pp. 7-13. DHHS No. (PHS) 82-1232. Public Health Service.
D.C.: U.S. Government Printing Office, 1981.
Washington,
current pregnancy.2 ° In sugary, anthropometric and obstetric
differences do not appear to account for the increased r isk of low
birthweight seen in blacks.
In trying to understand the nature of this r ask factor, it is
worthwhile to examine the low birthweight incidence among Mexican-
Americans, who are economically and sociodemographically similar in
some respects to black Americans, yet have been reported to have a very
low incidence of low b~rthweight. In 1979, 5.3 percent of Mexican-
, . _
Amer ican newborns weighed less than 2 , 500 grams, compared with 5.7
percent of white babies and 12.8 percent of black babies.2 ~ This low
incidence among Mexican-Amer loans is not readily explained. I t may be
due in part to problems in data reporting. Selby et al. recently
showed, for example, that the Spanish surname infant mortality rate may
appear lower than it actually is because of uneven reporting of infant
mortality in this population and that it is therefore an inaccurate
indicator of Mexican-American health status.2s Similar data problems
may skew reporting of low birthweight. The large difference between
black and Mexican-American low b~rthweight rates also raises the
possibili ty that cultural differences may play a role in pregnancy
outcome. The very low incidence of childbear ing among unmarr fed
Mexican-Amer ican women, unlike that among black women, and their
different dietary practices and family structures support this notion.
The forthcoming Hispanic HANES surrey should provide information on the
physical stature and health-related behavior of Mexi-can-Amer icans and
perhaps help to clarify the reasons for the low rate of low birt}1weight
observed in Mexican-ATner~cans.
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56
The issue of race and low birthweight is further complicated by the
different birthweight-specif~c neonatal mortality rates of white and
black infants that have been noted in a variety of populations. Black
infants born at less than 2,500 grams have long been recognized to have
better rates of survival in the neonatal period than low birthweight
white infants of similar birthweights.2 6 2 7
The conclusion to be drawn from the complicated data on race, low
birthweight, and race- and birthweight-specific mortality is that the
reasons for the risk differential between white and black neonates are
not well understood. The cumulative effects over time of poverty and
social neglect, and the interaction of such factors with biological
parameters, undoubtedly have played a role In these racial differences;
other factors remain to be defined. Research should be pursued to
obtain a better understanding of these issues.
Age
U. S. vital statistics data show that in 1978, 17 percent of all
births were to teenagers, yet 24 percent of all low birthweight infants
had a teenage mother.28 The relationship of low birthweight to age
was shown in Table 2.3 The rate for both whites and blacks is highest
at very young ages. It falls throughout the teenage years and reaches
its lowest point between 25 and 29 years. Thereafter, the low
birthweight rate rises slowly with increasing maternal age.
Teenage mothers, particularly the youngest (under age 15), have
many other risk factors that could be responsible for an adverse
pregnancy outcome. First births are more likely than later births to
be low-weight, and young mothers are more likely to be having their
first birth. However, when only first births are examined' teenagers
are still at higher risk than older mothers.22 Very young teenagers
having higher-order births are a particularly higher isk group, probably
in part because such births imply a short interval between pregnancies,
which itself Is a risk factor for low birthweight. Thirty percent of
second- and higher-order births to women less than 15 in 1978 were low
b~rthweight. Fortunately, there were fewer than 350 such births in the
United States in 1978.
Young mothers are more likely to be black and of low socioeconomic
status, to report late for prenatal care, and to be unmarrzed.28
They tend to be shorter and lighter than their older counterparts.29
Young teenagers, not being old enough to have completed their school-
ing, are less educated than older women. These factors in combination
appear to account for the higher rate of low birthwe~ght in teenage
mothers. For example, in one study, 422 consecutive prim~gravidas less
than 16 years old delivering at a hospital were matched by race to 422
primigrav~das aged 20 to 24 delivering at the same hospital. The
adolescent mothers delivered infants that were 40 grams lighter on
average than the young adult mothers, but the difference was not
statistically significant. It was noted that the adolescents were more
likely to be clinic patients, unmarried, and live In a census tract
with low buying power. They were shorter and lighter as well. When
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83
intervention. Important ones listed at the beginning of the chapter
include several sociodemographic factors; various medical and obstetric
risks; certain behavioral, environmental, and occupational factors; and
selected risks based in health care practices. It Is also apparent
that risks for low birthweight are widely distributed throughout the
population and that a substantial amount of low birthweight will
continue to occur outside of groups defined as high risk. This fact
highlights the need for greater understanding of r isk and etiology; it
should not be used to minimize the value of using existing r isk
information for targeting interventions.
Risk factor data also suggest another conclusion. Many of the
established risk factors are amenable to prevention or therapy, and of
these, many can be recognized before pregnancy occurs. Smoking Is
perhaps the best example. Other examples include poor nutr itional
status, certain chronic illnesses, and susceptibility to infections
such as rubella. Even demographic risk factors such as age can be
managed before conception, for instance, by avoiding pregnancy at
extremes of the reproductive age span; and the risks posed by high
parity and brief interval between pregnancies can be decreased through
family planning.
Another major conclusion that emerges from the literature on the
to answer
very long list of questions. Our understanding of the basic causes of
preterm labor and IUGR is seriously inadequate. A 1983 workshop
sponsored by the National Institute of Child Health and Human
Developments 6 ~ outlined promising research areas pertinent to IUGR,
and a recent review article by Huezar and Naftolint touches on a
etiology of low birthweight is that more research is needed
number of topics that should be studied to provide a better under-
standing of the normal onset of labor and of the pathogenesis and
process of preterm labor. In the absence of more complete information
about basic causal mechanisms, efforts to prevent low birthweight will
remain ~ zmited.
Factors whose role in low birthweight are uncertain need additional
analys is . Stress, for example, may be a s ignif icant r isk factor for
both IU=R and preterm labor, but more research is needed to understand
the nature and magnitude of this risk. Other possibilities that merit
study include, for example, the role of selected genitour inary
infections in low birthweight, the natural history of uterine activity
throughout pregnancy (to determine the value of uterine activity
assessment as an index in evaluating the risk of preterm labor), and
related topics mentioned in the section on evolving concepts of risk.
Well-established risk factors also require more attention. For
some factors, such as race, research is needed to understand why the
risk exerts its effect. For others, such as alcohol, the magnitude of
risk at various levels of consumption needs to be better defined.
For both known and less-certain r isk factors, efforts should be
made to distinguish risks for very low birthweight (1,500 grams or
less) from risks for moderately low birthweight (1,500 to 2,500 grams)
at various gestational ages. As Chapter 3 suggests, the incidence
trends and sequelae of these two classes of low birthweight differ.
Relating individual r isk factors to more ref. ined measures of low
birthweight should provide clues to both cause and prevention.
OCR for page 84
84
The committee's review of r isk assessment systems and instruments
suggests that they are helpful in distinguishing between h ~ gh- and
low-risk women. The significant incidence of low birthweight
deliveries in low-risk individuals and groups suggests, however, that
additional research is needed to improve the predictive capabil ity of
these systems. It also indicates that clinicians must be alert to the
possibility of low birthweight even in pregnant women judged to be at
low r isk of such an outcome.
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Representative terms from entire chapter:
preterm labor
