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OCR for page 96
Mechanisms for the Association of
Maternal Age, Parity, and Birth Spacing
With Infant Health
John G. Haaga
INTRODUCTION
Overview
This paper reviews possible biomedical mechanisms connecting maternal age,
parity, and birth spacing with infant mortality and assesses their likely importance
in accounting for the strength of these relationships as observed in household
surveys in developing countries. This is partly to help refine estimates of the
effects of family planning programs on infant health and partly to identify promis-
ing leads for research and the design and targeting of future maternal and child
health interventions.
In a review of studies using data from the World Fertility Survey (WFS),
Samuel Preston termed maternal age, parity, and birth spacing the "bio-demo-
graphic variables" affecting the risk of infant mortality (Preston, 1985, p. 265~.
Older studies using survey data and, to a lesser extent, data from vital events
registration systems had shown excess risks for infants born to very young and
very old mothers, for first births and for infants at very high birth orders, and for
infants born after (and sometimes before) very short interpregnancy intervals. In
the last decade or so analyses of demographic data, notably the WFS and similar
retrospective surveys in developing countries, using methods designed to over
John G. Haaga is policy analyst at the RAND Corporation, Washington, D.C.
96
OCR for page 97
INFANT HEALTH 97
come at least some of the methodological problems, have brought these risk
factors into new prominence. "Certainly the most surprising and probably the
most important new finding from the WFS," as Preston (1985) puts it, "concerns
the exceptionally high mortality rates among children born after a short birth
interval" (p. 266~.
Family planning programs can affect the distribution of all three of these risk
factors in the population and may thereby be an important tool in reducing infant
mortality rates. But the causal chains connecting family planning with the
ultimate outcome of life or death for an infant are long and complex. "Young
mother," "high parity," and "short interval" are not proximate causes of death
such as would be listed on a death certificate. Insofar as the associations observed
in demographic data are causal and not simply the result of confounding with
other social or biological factors, it must be because the biodemographic factors
increase the prevalence or severity of other conditions that are the more proximate
causes of death. This paper reviews the evidence for some of the more likely
mechanisms.
Even in low-mortality countries the large population-based studies that have
provided most of our knowledge about the risks associated with these maternal
factors (e.g., the Collaborative Perinatal Survey in the United States and the
British Perinatal Study) have not been analyzed in a way that would show which
direct causes of death are associated with the higher mortality rates for children
born to very young and very old mothers and those born at high parity and after
very short intervals. The WFS did not collect any information on causes of
death.) So for this paper most of the evidence about direct causes of death comes
from small clinical studies or special-purpose population studies, and their results
do not readily or entirely explain the mortality differentials associated with the
indirect factors that were measured in the demographic surveys.
None of the causal chains linking maternal characteristics with more direct
risk factors and ultimately to poor pregnancy outcomes and infant deaths is
entirely understood at the organ system or cellular level. For example, one can
observe relationships between anemia or certain maternal infections and prema-
ture onset of labor, but it is not known what triggers labor or exactly how these
maternal conditions affect the process. And the associations for which the
evidence is strongest and the relative risks highest (notably the link between older
maternal age and chromosomal abnormalities) are less important as causes of
infant death in poor countries than in rich ones. A large part of the work for this
paper consisted of culling results from obstetric, biological, and epidemiologic
studies in rich countries and guessing their public health significance for poor
countries.
awe Demographic and Health Surveys are collecting retrospective cause-of-death information in
one country on an experimental basis.
OCR for page 98
98 JOHN G. HAAGA
There have been a few good longitudinal field studies following infants from
before birth in developing countries. But the logistical problems of maintaining a
study group and obtaining accurate measurements and cause-of-death reporting
preclude large samples. There are some interesting hospital-based studies, but
these are always subject to severe selection and ascertainment biases in environ-
ments where most mothers and children do not get adequate care.
The remainder of this section discusses in more detail the differences between
high- and low-mortality countries in the causes of in&et deaths, which have a
large influence on my subjective estimates of the likely importance of the causal
mechanisms outlined in the rest of the paper. Next I list the possible causal
mechanisms for which there is some evidence of association with young maternal
age and primiparity. Then I discuss mechanisms that may link old mammal age
and high panty with infant health. Finally, possible mechanisms for the effect of
short interpregnancy or interbirth intervals on infant health are discussed.
To avoid repetition, maternal nutrition and infectious diseases are discussed
only briefly in the second and third sections, which deal with maternal age and
parity. They are dealt with more fully in the fourth section, on the effects of short
intervals between pregnancies, for which their relevance is judged to be greater.
Causes of Infant Deaths
The pregnancy conditions for which evidence of an association with biode-
mographic variables is strong are not usually very important as causes of infant
deaths in poor countnes. Conversely, the major proximate causes of infant deaths
in poor countries are not clearly related to biodemographic variables.
The causes of infant deaths differ between high- and low-mortality environ-
ments. It is difficult to obtain accurate information on causes of death when, as in
most high-mortality countries, the majority of deaths are not attended by trained
health workers. Even in low-mortality countries where most deaths occur in
hospitals and there are strict requirements for certification, recording of causes
can be unreliable and it can be difficult even to decide what is meant by cause of
death in most situations, if a single cause must be chosen and recorded. But there
is a reasonably clear picture of differences between high- and low-mortality
countries, at least when causes of death are grouped into very broad categories.
Table 1 presents data on the causes of infant deaths in two reasonably well
documented cases, corresponding to high- and low-mortality environments: (1)
Recife, Brazil, in the late 1960s, when a special effort was made as part of the
Inter-American Investigation of Mortality in Childhood to notify medical authori-
ties and gather information on infant deaths as soon as possible after their
occurrence and (2) the United States in 1983. Infectious and parasitic diseases
account for a much larger proportion of the total when infant mortality rates are
high. The lower the overall infant mortality rate is, the higher the proportion of
OCR for page 99
INFANT HEALTH 99
TABLE 1 Percentage of Infant Deaths by Cause: Recife, Brazil, and United States
Recife, Brazil United States
1968-197 1a 1983
Infectious and parasitic diseases 51 2
Diseases of the respiratory system 11 4
Congenital anomalies 4 21
Certain pennatal conditions 26 47
Ill defined 8 14
All other - 11
Total 100 100
Infant mortality rate per
1,OOOlivebir~s 91 11
a"Basic causes" only (from Inter-Amencan l~vesiiganon of Monality in Childhood).
Sources: Puffer and Serrano (1973), WHO (1987).
deaths attributable to congenital anomalies and to "certain conditions originating
in the perinatal period," including birth trauma, hypoxia, and "immaturity."2 And
of the deaths due to these conditions, it is likely that a higher proportion of those
in poor countries are attributable to poor obstetric care than to the age- and parity-
related causes predominant in rich countries. For example, in the Narangwal
study in the Punjab, 9 of the 24 deaths ascribed to "intrauterine asphyxia" were
associated with administration of pytocin by indigenous practitioners to speed up
labor (Kielmann and Associates, 1983, p. 197~.
This contrast is important in the present context because it indicates the
relative size of the effects that would have to be present for a particular category
of cause of death to account for the observed indirect relationships between
biodemographic variables and infant mortality. For example, if the effect of a
short birth interval is associated with a relative mortality risk of 1.5 (relative to
standard risk of 1.0 for births occurring after intervals of 2 to 4 years), and if this
association is entirely causal and operates through only one of the categories of
cause shown in Table 1 (an artificial and unlikely assumption), then a short bird
interval would have to raise the risk of death from infectious and parasitic
2The figures shown in Table 1 are percentages of deaths corresponding to very different levels of
infant mortality, of course. The modality rate due to congenital abnormalities in Recife (4 percent of
9 1 per 1 ,000, or just under 4 deaths per 1,000 births) was higher than the same rate in the United States
(21 percent of 11 deaths per 1,000, or just over 2 deaths per 1,000 births).
OCR for page 100
100 JOHN G. HAAGA
diseases by a factor of about 2. But a short birth interval would have to raise the
risk of death from congenital anomalies by a factor of about 50 to account for the
whole indirect association between short intervals and infant mortality. This
alone makes it more likely that increased susceptibility to infectious disease,
rather than increased incidence of congenital anomalies, is the most important
underlying cause for the associations between biodemographic variables and
infant mortality.
Low Birthweight and Prematurity
Low birthweight is associated with a higher risk of infant mortality, morbidity,
and developmental problems (IOM, 1985~. Infants may be small because they
were born at less than full term (before the thirty-seventh week of pregnancy,
counted from last menstruation, is a commonly used cutoff) or because they were
born at full term after poor growth during uterine life (intrauterine growth retarda-
tion, or IUGR). Different combinations of gestational age and weight at birth are
associated with different levels of risk to the infant.
Low birthweight and prematurity have many causes, and it is likely that the
risk posed by a given deficit varies according to what caused it. The sections that
follow discuss the limited evidence relating various biodemographic factors to
birthweight and prematurity.
In relative terms, prematurity3 accounts for a larger proportion of low birth-
weight infants in rich countries than in poor countries, where many more infants
born at term are low in weight (Villar and Belizan, 1982~. The relative risk of
infant mortality is much higher for the preterm Ban for the term-but-low-weight
infant. This point was brought out very starkly by a recent study of hospital births
in Mexico City and Santa Cruz, Bolivia: the risk of neonatal mortality for preterm
babies (relative to babies born at term and weighing more than 2,500 grams) was
24 and 100, respectively, in the two sites, compared to relative risks of 4.0 and
3.3, respectively, for babies born at term but weighing less than 2,500 grams
(Haas et al., 1987~. But the etiology of prematurity is still largely a mystery
(Alger and Pupkin, 1986~. In an interesting exercise in apportioning the at~but-
able risk of low birthweight and prematurity, and Be relative risk in rich com-
pared with poor countries, among different proximate determinants, Kramer
(1987) found that only about a quarter of variation in prematurity could be
"explained" and much of that was with relatively uninformative determinants
such as "nonwhite race."
3I use the term prematurity and the adjective prefers only to mean early labor and delivery,
usually defined with a cutoff of 37 weeks' gestation, counted from last menstruation. In older
literature prematurity was often used for any low binhweight.
OCR for page 101
INFANT HEALTH 101
YOUNG MATERNAL AGE AND PRIMIPARITY
Effects on Birthweight and Prematurity
In the United States infants born to young mothers are at increased risk of
premature delivery, low b~rthweight, prematurity, and pennatal death. Table 2
shows the relative risks of (1) birthweight less than 2,500 grams and (2) 5-minute
Apgar scores (a composite index, including several signs associated with prema-
tunty) less than 7 by mother's age for infants born in the United States in 1983. It
can be seen that the risks of poor pregnancy outcomes are higher for younger
mothers and that they are especially high among mothers less than 15 years old.
In high-mormlity countries as well, infants born to young mothers are often at
a disadvantage. In five of the Latin American project sites for the Inter-American
Investigation of Mortality in Early Childhood in 1967-1970, infants born to
mothers less than 20 years old were between 1.3 and 1.9 times as likely to die in
the neonatal period as those born to mothers aged 20 to 24, and their relative risk
was about as large for postneonatal deaths as well (Puffer and Serrano, 1973,
Table 147~. This was entirely associated with age, not primiparity, since a more
detailed analysis showed that within mother's age categories first-parity births
had the lowest neonatal death rates of all parities in most of the sites (Puffer and
Serrano, 1975~.
A more common finding is that primipanty is a risk factor for poor pregnancy
outcomes over and above the effects of maternal age. The Collaborative Pennatal
Study in the United States found that average bir~weights were lowest for first
births for both black and white infants born in 15 university-affilia~d medical
TABLE 2 Risks of Low Binhweight and Low 5-Minute Apgar Scores, by Age of Mother, United
States, 1983
Mother's Age
(years) BW <2,500 grams 5-minute Apgar<7
< 15 14.5% 4.1%
15 12.0 3.2
16 10.7 3.0
17 10.0 2.8
18 9.4 2.6
19 8.4 2.4
2(}24 7.0 2.0
Source: National Center for Health Statistics, Advance Report of Final Natality Statistics, 1983
(Monthly Vital Statistics Report, September 1985).
OCR for page 102
|02 lOlIN G. HAACA
centers in the years 1959-1965 (Table 3~. Perinatal death rates (late fetal deaths
plus deaths in the first week of life) were higher for first pregnancies than for
second ones, although they tended to increase thereafter with parity. Neonatal
death rates tended to increase, although not necessarily monotonically, with parity
Niswander and Gordon, 1972~.
By contrast, in data from developing countries, first births do not consistently
appear at a disadvantage. In a review of results of the WFS, Preston (1985) found
the evidence for an excess mortality risk for first births equivocal. He suggested
that in retrospective surveys women may tend to underreport first births of
children who later died. The Inter-American Investigation of Mortality in Child-
hood, in which data were collected shortly after the time of death (and thus
presumably would have been less subject to the type of recall bias Preston
suggests), found that first births had the lowest mortality rates, within categories
of mother's age, in the four project sites for which data were disaggregated-
Chile, Mexico, Canada, and the United States (Puffer and Serrano, 1973, Table
151~.
Mojarro and Aznar (1986) present infant mortality rates from rural Mexico by
mother's age and parity '(Table 4~. They show that the excess risk for infants born
to mothers less than 20 years old was for the second and third infants. Presumably
a relatively high proportion of these babies are born after a relatively short birth
interval and/or after a short gestation (a woman who gives birth for the first time
at age 16 does not have enough time to 'have her third child before age 20, if she is
to have the low-risk 2-year interval between births). In these data, infant mortal-
ity was actually higher for first-parity births to mothers aged 20 to 24 than for
mothers less than 20. But the studies from rich countries showing the excess risk
for the "older pnmipara" usually use the 20- to 24-year-old mothers as the refer
TABLE 3 Birthweights and Perinatal and Neonatal Death Ratios by Parity and Race, United
States, 1959-1965
Mean Birthweight Pcrinatal death Neonatal death
(grams) ratios
Whites Blacks
Parity
rates
Whites Blacks Whites Blacks
0 3,234 2,960 29 40 11 lS
1 3,290 3,029 26 39 12 20
2 3,288 3,074 40 41 15 23
3 3,291 3,097 44 37 18 17
4 3,306 3,107 52 42 16 18
5+ 3,340 3,138 61 51 20 23
Source: Niswander and Gordon (1972).
OCR for page 103
INFANT HEALTH ~ 03
TABLE 4 infant Mortality Rates by Panty and Mother's Age, Rural Medico, 1965-1974
Panty
First 2-3
4 ~7+ Total
Mother's Age
~ 2069 106a a 86
2(}24108 65101 a 83
2~29a 5675 84 72
3(}34a a75 79 77
35a 99 100 101
Total84 7484 89 83
Note: n = 551 infant deaths, 6,640 live births.
aFewer than 10 deaths in call.
Source: Moja'To and Amer (1986, Table 8.3).
ence group with optimum conditions for childbearing. I suspect that the 20- to 24-
year-old primiparae represented in the rural Mexican data include a large number
of women who had prior miscarriages. The lowest infant mortality rates in this
high-fertility population, in fact, are found along the diagonal of the table: these
represent the women who are having the `'right" number of live births for their age
group.
Some of this difficulty could be removed if data were always available that
separated the effects of panty (number of prior live births from gravidity (number
of prior pregnancies), but fetal losses are underrepresented in both survey and
certificate data, especially in high-mortality countries. The difference between
the American and Mexican maternal age comparisons illustrates an important
difficulty in making comparisons across populations of the effects of biodemogra-
phic variables on infant mortality. Since there are no random controlled trials
(one cannot assign women to different parities at different ages), powerful social
influences on the timing and pace of childbearing cause selectivity biases that are
only partially and imperfectly controlled by the socioeconomic-status variables
usually available. The biases vary among societies in magnitude and even
direction.
It is difficult to separate in analyses the pure effects of young maternal age and
primiparity from the effects on infant health of other factors associated with
young motherhood and first parity in different societies. Especially in high-
fertility countries, primiparous women are an increasingly select group in each
older age group: women in their thirties giving birth for the first time have often
had one or more previous pregnancies terminated by miscarriage or induced
abortion. (A similar situation exists in sorting out the effects of old maternal age
and "grand multiparity," though there is more variation at the end than at the
OCR for page 104
104 JOHN G. SAGA
beginning of reproductive careers, and the sample size, collinearity, and selectiv-
ity problems for statisticians are somewhat more tractable.) For the purposes of
this review, the distinction between effects of young motherhood and effects of
primiparity is quite important. Family planning programs can be expected to
reduce the incidence of births to young women. But the proportion of all births in
a population that are first births would likely increase as a result of widespread use
of contraception to limit family size (Bongaarts, 1987~.
Young maternal age is also confounded by environmental and possibly genetic
characteristics that can affect infant health independently. In the United States,
for example, young mothers are disproportionately black, poor, unmarried, and
uneducated. They are less likely to receive antenatal care early in pregnancy than
are older mothers, and the care they do get is often disjointed. Three recent
reviews of the literature on the health consequences of adolescent pregnancy in
the United States have all come to very similar conclusions (Strobino, 1987;
Geronimus, 1987; McAnarney, 1987~. As Strobino (1987) puts it, "adolescence,
per se, may not be a risk factor for poor health outcomes of the mother or her
offspring, but rather . . . the preponderance of other risk factors such as low
socioeconomic status, poor prenatal care and primiparity is the reason for their
poor outcomes" (p. 111).
To some extent this conclusion also holds for high-mortality countries, even
though adolescent childbearing is not such a deviant behavior elsewhere as it is in
the United States. Barros et al. (1987a, 1987b), for example, found higher rates of
both perinatal and neonatal mortality among infants born to mothers less than 20
years old in a small city of southern Brazil. The mortality differences between
these infants and those of mothers aged 20 to 29 completely disappeared when
family income and whether the woman received antenatal care were controlled.
DaVanzo et al. (1984), using recall data from a household survey in Malaysia,
found that first births weighed significantly less than higher-order births. They
found a positive bivariate association between mother's age (up to 35 years) and
birthweight. The association between first-birth order and low birthweight per-
sisted in a multivariate analysis controlling for family income and other social
characteristics, while the association between young maternal age and low birth-
weight disappeared in the multivariate analysis. In an analysis of determinants of
infant mortality using the same data, younger maternal age (below 18 years) was
associated with increased risk of infant death, but the association was much
diminished when social characteristics and behavioral variables (notably breastfeed-
ing) were controlled (DaVanzo et al., 1983~.
The results of these Brazilian and Malaysian analyses tend to support the
conclusion that young maternal age is less important than primiparity as a risk
factor for low birthweight and infant mortality. It may be that very young
maternal (gynecologic) age poses great risks to the infant, but in the studies
reviewed for this paper the age cutoffs used to define young maternal age were
sufficiently high that the excess (relative) risk was small. Small sample sizes in
population-based studies typically preclude estimation of infant mortality risks
OCR for page 105
INFANT HEALTH 105
for very young mothers, which means that this potential risk factor is not a major
attributable risk for infant mortality in the countries for which we have good
information.
The remainder of this section examines in turn the major pathways or proxi-
mate causes through which young maternal age could be associated with lower
birthweight and infant deaths.
Mother-Fetus Competition for Macronutrients
It is generally thought that girls are still growing for 4 years after menarche
and that the energy cost of a pregnancy during these 4 years must compete with
the energy cost of linear growth of the mother (NRC, 1970~. In analyzing data
from the Collaborative Perinata1 Study, Naeye (1983) showed that infants born to
very young (10- to 16-year-old) black mothers had low birthweights and lengths,
which he suggested could be explained by the "fetal-maternal competition for
nutrients." And in an analysis of data on infants of very young black mothers in
New Orleans, Cherry et al. (1987) showed that this birthweight and length deficit
persisted through infancy into childhood. But other studies have shown that for
most girls the linear growth spurt in adolescence takes place well before menarche
or during a period of adolescent subfecundity (see McAnarney, 1987, for a
review). The energy cost of linear growth is a fairly small percentage of meta-
bolic requirements even for young children, and linear growth is interrupted
quickly when there is nutritional stress. In any case, as discussed further later in
this paper, the energy costs of pregnancy are surprisingly low and can usually be
met at the expense of maternal fat deposition even during nonharvesting seasons
in very poor communities in West Africa.
On the face of it there appears to be little reason to think that absolute shortages
of macronutrients are a binding constraint on fetal growth. except in the most
extreme circumstances. McAnarney (1987) suggests that the small size of the
infants born to very young mothers in the United States is more likely due to the
mother's small size at maturity, before pregnancy, and to their greater rates of
infection and premature delivery than to a simple competition between two
growing children, one in the womb of the other. It may also be that the problems
arts not ~ match with the. `~nntilv of nutrients in the mother's circulatory system
~ ·-~- vie ~ ' ^~ ~- ~
as with the size and development of the uterine blood vessels early in pregnancy:
a fetus can be undernourished even when there are "enough" nutrients around if
the maternal-fetal transfer is impaired.4
The situation may be different in poor countries. Age at menarche occurs later
4I discuss This point further below in discussing short spacing between pregnancies. This point has
been made in connection with studies of placenta morphology and IUGR in general, but my connec-
tion of it to the specific problem of adolescent pregnancy does not have any other support in the
literature.
OCR for page 106
106 JOHN G.HAACA
on average in poor countries than in Northwest Europe and North America, where
secular declines in age at menarche have been documented. At the same chrono-
logical age, teenagers in poor countries are usually at a younger gynecologic age
than their contemporaries in rich countries Growth may last longer after me-
narche as well.5
My tentative conclusion is that the evidence is weak for an effect of young
maternal age on fetal growth and infant health through direct competition for
nutrients. More plausible is an association caused by the connection of both very
young maternal age and poor infant health with poverty and poor sanitary condi-
tions. There is little evidence directly bearing on the issue of young mothers, but
it could also be that "uteroplacental perfusion" of nutrients is impaired in very
young women, as it appears to be in animal studies of undernutrition in preg-
nancy.
Micronutrient Deficiencies
Iron and folate deficiencies are common in pregnancy, and routine supplemen-
tation is recommended by the World Health Organization (WHO). In the United
States, teenage mothers are often found to be more anemic than older mothers, but
this effect is most likely due to their poverty and poor diets rather than to any true
age effect (Strobino, 1987~. The more common finding in poor countries appears
to be an association of iron and folate deficiencies in high-parity pregnancies
(anemia is discussed in greater detail later in this paper.
Zinc is a micronutrient that has attracted a great deal of attention in recent
research (Swanson and King, 1987~. It is suspected that one of the ways in which
maternal smoking and alcohol intake affect fetal growth is by interfering with the
mother's zinc utilization. Whether because of these behaviors or because of
dietary deficiencies, low circulating zinc levels have been found in pregnant
teenagers in the United States. Pregnancy-induced hypertension and poor preg-
nancy outcomes (e.g., prematurity, IUGR, congenital malformations) have been
associated in observational studies with low circulating zinc levels, but so far
results of supplementation trials are equivocal. Apparently the assessment of zinc
status is extremely difficult, and the studies reviewed by Swanson and King have
all been conducted in low-mortality countries. For the purposes of this paper, zinc
deficiency must be considered a factor that may prove an important link between
slbis is at least a possibility. It is known that children in poor communities, where undernutrition
and infectious diseases are prevalent, are shorter than those of similar genetic background who have
had less stress, at least until the age of 7 or so. But adults in poor countries (e.g., West Africa) are not
much smaller than those from rich countries. It has been suggested that linear growth lasts longer (say,
into the early twenties) to account for this discrepancy (Habicht et al., 1974). This might prolong the
period between menarche and the end of linear growth.
OCR for page 129
INF^T HEALTH 129
infectious agents are cytomegalovirus (CMV), rubella, hepatitis B. and herpes
simplex. Except for rubella, which is transmitted only to the fetus, each can result
in a congenital, intrapartum, or postnatal infection in the infant. CMV and herpes
simplex virus have been associated with many negative outcomes for the fetus/
neonate: fetal death, prematurity, IUGR, malformations, congenital infection,
acute postnatal infection, and persistent postnatal infection. Rubella is associated
with all these except acute postnatal infection. Hepatitis B (which is endemic in
many developing countries, e.g., in Southeast Asia) also has been linked to
prematurity and fetal and neonatal infectious disease (Overall, 1987~.
Nonviral maternal infections are less likely to cross the placenta, but they may
still affect the fetus before or during labor, especially if the membranes have
ruptured prematurely.
Premature rupture of the membranes (PROM) and preterm labor in general
pose a severe risk of infant mortality. Infants born after PROM are at increased
risk of neonatal infections, perinatal asphyxia, and respiratory distress syndrome
[though for the latter the risk associated with PROM is less than that associated
with other types of premature labor (Blackmon et al., 1986~. "Neither the
etiology of premature rupture of the membranes nor of premature labor is known.
However, a growing volume of experimental and clinical data strongly supports
genital infection either directly or indirectly as a major cause of both" (Alger and
Pupkin, 1986:760~. Genital infections are more common among poor and unedu-
cated women than among those with better access to health care and those who
practice better hygiene. To the extent that the high-risk groups defined by the
biodemographic variables include more poor women, they can be expected to
experience premature labor more often, with negative consequences for the neo-
nate.
Maternal parasitemias fungal or bacterial infections that can affect the fe-
tus include toxoplasmosis, syphilis, tuberculosis, and trypanosomiasis.~7 In
general, congenital infections may produce symptoms at birth, but in the majority
of cases they are insidious, producing symptoms after some months (Berkowitz,
1984~. Presumably even a congenital infection that is not itself a leading direct
cause of infant deaths may render the infant more susceptible to later infection.
Ascending infections to which a baby is vulnerable after the membranes have
broken include septicemia and pneumonia. During a baby's passage through the
birth canal, she or he is susceptible to infections of the mother's urinary tract,
including CMV and fecal bacteria (Berkowitz, 1984~.
Most of these infections are prevalent in developing countries. CMV is very
widespread in both rich and poor countries; one source estimates that the preva-
lence of CMV seropositivity in women ranges from 8 percent to 60 percent
worldwide (Peckham et al., 1987~. CMV has been called "a significant pathogen
~7Malana is discussed separately above.
OCR for page 130
i 30 JOHN G. HAAGA
of the human fetus capable of producing disease ranging from subtle abnormali-
ties not detectible at birth to severe multisystem disease" (Wright, 1980, p. 170~.
On the other hand, "the fate of infants born with asymptomatic CMV is not clear"
(Wright, 1980, p. 170~. Rubella is highly communicable and has been shown to
cause severe fetal abnormalities. Unnary tract infections, very common in poor
countries and among poor people in rich countnes, are associated with a sharply
increased likelihood of low birthweight (due to prematurity, IUGR, or bother
Sever et al. (1977) matched pregnancies in the Collaborative Pennatal Survey in
the United States by maternal age, race, birth institution, and socioeconomic
status and found a relative risk of 3.7 for stillbirths to women with urinary tract
infections; 1.5 for a birthweight of 2~000 to 2,499 grams; 2.8 for a birthweight of
1,500 to 1,999 grams; and 4.5 for a birthweight below 1,S00 Cams. Gazaway and
Multus (1986) reported a relative risk of preterm labor of 3.8 in pregnant women
with bacterial vaginoses compared with those without it.
What is missing for almost all of these congenital infections is strong evidence
that maternal exposure or susceptibility is related to biodemographic variables.
Older mothers (and grand multiparae?) are known to suffer a greater incidence of
PROM, which may increase the risk of intrapartum infections. There is evidence
that malaria in particular affects the growth of the fetus and the transmission of
maternal immunoglobin at parity 1 (see above).
Of the other infectious agents, CMV is a good candidate for more research.
There are recent studies from Britain and the United States that show the ease with
which it can be passed in either direction by a nursing mother and an infant, and
older siblings may bring CMV home from day care settings and infect their
pregnant mothers (Peckham et al., 1987~.
Increased Postnatal Exposure to Pathogens
The two most common routes for postnatal infections are fecal-oral and
respiratory-respiratory (Chen, 1983; Stanfield, 1987~.~8 A child born at high
panty is likely to live with many siblings, and if the births have been closely
spaced, these will be young siblings. A child born within a year after the previous
child will reach the age at which immunities acquired across the placenta or
~ - e most common deadly disease transmitted otherwise than these two routes is neonatal
tetanus, usually caused by septic cutting and sealing of the umbilical cord. Stanfield and Galazka
(1984) summarized community surveys of causes of infant deaths, mostly from South Asia and Sub-
Saharan Afnea, showing that about 20 to 40 percent of neonatal deaths in these high-mortality regions
are caused by tetanus. I found no literature showing any relationship between tetanus infection and the
biodemographic variables of interest. Ronald Gray (personal communication) teas suggested that there
may be a link due to a lower likelihood of some pregnant women (e.g., young women, primiparae)
receiving antenatal tetanus immunization. If so, this would represent another case in which the
biodemographic variables are markers for social factors affecting maternal and child health, rather
than causal factors.
OCR for page 131
INFANT lIEALTH 131
through breast milk (3 to 9 months) when the next older sibling has become
mobile and is likely to be in contact with all sorts of pathogens (15 to 21 months).
Some studies of measles mortality in rural and periurban Guinea-Bissau have
showed that crowding, specifically the number of other children in a household, is
a better predictor of measles mortality than are anthropometric indicators of
nutritional status (Aaby et al., 1983; Smedman et al., 1987~. Though they do not
report causes of death by birth order, the authors of the summary report on the
Narangwal experiment in maternal and child health services in the Punjab report
excess mortality among children above both order seven (twice the rate for the
whole sample), with most deaths in the sample caused by gastrointestinal and
respiratory infections (Kielmann and associates, 1983~.
Infections transmitted via feces are very important as causes of infant deaths
and may be facilitated by the presence of many children, especially young ones, in
the household. A recent study showed that 55 percent of cholera cases in
Bangladeshi villages could be attributed to the excess risk posed by having an
asymptomatic breastfeeding child who has cholera vibrio in her or his stools
(Riley et al., 1987~. Riley et al. surmise that careless handling of an infant's feces
facilitates transmission. This would be a specific reason for young siblings, rather
than just many siblings, being a risk factor, which would account for an associa-
tion of close birth spacing with infant heals. Similarly, another study from the
International Center for Diarrheal Disease Research in Bangladesh (apparently of
different villages) found infant mortality to be higher in households with more
than 10 members than in smaller households a relative risk of 1.5 in an analysis
controlling for several other economic and demographic variables (Rahman et al.,
1985~. In this sample, the authors argue, such large households tend to have more
than two adult earners and thus are not poorer than smaller households, thus
reversing one effect that confounds crude household-size mortality differentials in
other samples. Diarrheal diseases were the leading cause of infant morbidity and
mortality in this sample, and the authors suggest that careless handling of the
feces of small children explains the significant effect of household size. Yet
another analysis from the same institution showed specifically that the presence
of other children in the household who are less than 5 years old was associated
with worse nutritional status as measured by anthropometry for boys (though
apparently not for girls), even when measures of social and economic status were
controlled (Becker et al., 1986~. This finding is compatible with any of the three
effects discussed here-prenatal nutrition, postnatal nutrition, and infectious dis
ease.
Conclusions
Of the biodemographic risk factors discussed here, the state of knowledge
about intermediate mechanisms for short interpregnancy intervals is the least
satisfactory. This is especially unfortunate because the direct impact of family
OCR for page 132
~32 lOHNG. H^GA
planning programs on infant health (apart from their association with prevention
of unwanted births and better provision of maternal and child health services) is
expected to come about largely from a decrease in the number of exceptionally
short intervals.
In my view the best evidence is for some mechanism interfering with the
development in early pregnancy of the uteroplacental circulatory system, leading
to fetal growth retardation. There may also be problems with reproductive tissues
(e.g., cervical incompetence' which leads to premature delivery). This latter
mechanism could, at the same time, be a sort of statistical artifact (short intervals
just happen to include more of the infants born, for unrelated reasons, after short
gestation) and a true causal chain inadequate recuperation from the first partun-
tion, leaving structures too weak to support the next pregnancy. The WFS studies
have found short intervals to be associated with an excess risk that continued well
past early infancy, but this is consistent with both prematurity and fetal growth
retardation as causal mechanisms, since infants born too small and too early who
survive the neonatal period may still have respiratory and immunologic problems
that weaken them later.
A high priority for further research should be the collection of information on
birthweights, gestational ages, and causes of death in association with data on
pregnancy intervals (preferably entire reproductive histories). This includes
many variables that are extremely difficult to collect in field studies, of course,
but the selectivity of hospital samples may be too great in populations where the
attributable mortality risk is high enough. Where demographic surveillance
systems are in place, a useful study design might be a case control, matching each
short-interval death with a normal-interval death and comparing proximate causes,
ages at death, and risk factors.
It would be interesting to isolate the effect on infant health of a "pure"
reduction in the proportion of short interpregnancy intervals, unaccompanied by
changes in women's education, their social roles, access to other health services,
etc. Insofar as family planning programs actually do bring about a reduction in
the proportion of short intervals, measuring this effect would allow us to estimate
the benefits in terms of child health of increased effort in family planning pro-
grams. (We are leaving aside the effect of family planning programs on the
number of dependents in each chills family and thus the number of competitors
for presumably limited health-related resources.)
The very success of a family planning program in a new geographic area or in
a poorer social class provides evidence that women's roles and their ability and
willingness to use health-related resources and knowledge, among other things,
have changed and are changing. To some extent the effects of confounding and
unobserved variables on estimating the effect of interval length on infant mortal-
ity can be alleviated by better measurement of social, economic, and other health-
related variables and by careful specification of statistical models. Such research
OCR for page 133
INFANT HEALTH ~ 33
will help policymakers assess the most effective mix of components of health
services (including family planning) in different settings.
ACKNOWLEDGMENT
I received very helpful advice, comments, and references from many members
of the worldling group and from others who reviewed earlier drafts of this paper. In
particular, I would like to thank Julie DaVanzo, Peter Donaldson, Judith Fortney,
Ronald Gray, Jorge Martinez-Manatou, Anne Pebley, Joseph Potter, and James
Trussell for all of their assistance.
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1983
Representative terms from entire chapter:
infant mortality
