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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

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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.

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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

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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).

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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.

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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).

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|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).

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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

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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

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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.

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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.

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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.

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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.

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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

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~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

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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. REFERENCES Aaby, P., J. Bulsh, I. M. Iisse, and A. J. Smets 1983 Measles mortality, state of nutntion, and family structure: a community study from Guinea-Bissau. Journal of InfcctiousDiscases 147:693-701. Alberman, L 1984 Alger, L S., and M. J. Puplcin Low bi~hweight. Pp. 8~98 in M. B. Bracken, ed, Pcrinatal Epidemiology. New York: Oxford University Press. 1986 Etiology of preterm premature rupture of the membranes. Clinical Obstetrics and Gynecology 29:758-770. Allen, G. 1984 Multiple births. Pp. 152-189 in M. B. Bracken, ea., Perinatal Epidemiology. New York: Oxford University Press. Anderson, G. D., and B. Sabai 1986 Hypertension in pregnancy. Pp. 819 863 in S. G. Gabbe, J. Niebyl, and J. L Simpson, eds., Obstetrics: Normal and Problem Pregnancies. New York: Churchill Iivingstone. Balclceteig, L S., and H. J. Hoffman 1979 Perinatal modesty by birth order within cohorts based on sibship size. British Medical Journal 2:693 696. Barros, F. C., C. G. Victora, J. P. Vaughan, A. M. B. Temera, and A. Ashword~ 1987a Infant mortality in southern Brazil: a E-aiion-based study of causes of death. Archi~cs of Diseases in Childhood 62:487~90. Barros, F. C., C. G. Victora, J. P. Vaughan, and H. J. Estanislau 1987b Pennatal matality in southern Brazil: a poE~aiion-based study of 7392 births. WHO Bulletin 6S:9S-104. Becker, S., R. E. Black, K. H. Brown, and S. Nahar 1986 Relations between studio economic status and morbidity, food intake and growth in young children in two villages in Bangladesh. Ecology of Food and Nutrition 1 8:251-264. Berkowitz, I. D. 1984 Infections in the newbom. Pp. 59-80 in M. Ziai, T. A. Clarice, and T. A. Merritt, cds., Assessment of the Newborn: A Guide for the Practitioner. Boston: Idle, Brown. Blackman, L, L S. Alger, and C. Crenshaw 1986 Fetal and neonatal outcome sassonated with premature rupture of the membranes. Clinical Obstetrics and Gynecology 29:779-815.

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~ 34 JOHN G. HAACA Boerma, J. T., and H. van Wienen 1984 Binh interval, mortality and growth of children in a rural area of Kenya. Journal of Biosocial Science 16:475~86. Bongaarts, J. 1987 Does family planning reduce infant mortality rates? Population and Development Review 13:323-334. Brabin, B. J. 1983 An analysis of malaria In pregnancy in Africa. Bulletin of the WHO 61:1005-1016. Bray, R. S., and M. J. Anderson 1979 Falcipa~um malaria and pregnancy. Transactions of the Royal Society of Tropical Medicine and Hygiene 73:427~31. Bnend, A. 1985 Normal fetal growth regulation: nutritional aspect". Pp. 1-22 in M. Gracey and F. Fawner, eds, Nutritional Needs and Assessment of Normal Growth. Nestle Nutrition Workshop Series Vol. 7. New Yodc: Raven Press. Chen, L. C. 1983 Child survival: levels, trends and determinants. Pp. 199-232 in R. A. Bulatao and R. D. Lee, eds., Deternunants of Fertility in Developing Countries. Supply and Demand for Children, Vol. 1. New York: Academic Pregg Cherry, F. P., P. Mather, and N. Mock 1987 Long tend effect of gynecologic age on somatic growth of children. Journal of Community Health 12:108-116. Costello, C. 1986 Matemal and Child Health in Rural Uganda: We Role of Nutrition. Ph.D. disserta tion, University of Pennsylvania Crowther, C. A. 1986 A prospective study of hypertension in pregnancy at Harare maternal hospital. Central African Journal of Medicine 32:175-180. DaVanzo, J. S., and E. H. Starbird 1989 Correlates of Short Inter-Birth Intervals in Malaysia: We Roles of Breastfeeding and Contraceptive Use. Paper presented at meetings of the Population Association of Amenca, Baltimore Md., March. DaVanzo, J. S., W. P. Butz, and J. P. Habicht 1983 Biological and behavioral influences on the mortality of Malaysian infants. Population Studies 37:381~2. DaVanzo, J. S., J. P. Habicht, and W. P. Butz 1984 Assessing socioeconomic correlates of birihweight in peninsular Malaysia: ethnic differences and changes overtime. Social Science and Medicine 18:387~04. Davies, A. M., and W. Dunlop 1983 Hypertension in pregnancy. Pp. 167-208 in S. L. Barron and A. M. Johnson, eds, ObstetricalEpidemiology. London: Academic Press. Erring, E. I., and M. O. Banjoko 1975 the obstetric perfonnance of Nigerian priniigravidae aged 16 and under. British Journal of Obstetrics and Gynecology 82:228-233. Ferraz, E. M., R. H. Gray, P. L Fleming, and T. M. Maria 1988 Interpregnancy interval and low birth weight: findings from a case-control study. American Journal of Epidernlology 128:1111-1116. Fleming, P. L., and R. H. Gray 1988 Some effects of the preceding birth interval on bi1th weight and subsequent growth. Mimeo, Department of Population Dynamics, Johns Hopkins University, Baliirnore, Md.

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_~~ 135 ~_ 1983 we ^= ~ ~ ~ ~ sit ad it wait By. 11~126 ~ ha. P=s, B. ant, ad 1. A. Fat, as., COMA i~ Dev.~g ~. Bose: Repass. Fat, J. A., 1. E. ages, A. ~z~e, F. Ham, L. G. it, ad I. Be 1983 ~_~age35: ~e. ~.3-15~. Pals, B. ant, ad J. A. Fly, as., ~- ~ Devout' a. ~ Repass. F~,J. A., J. E. Its, K. I. Kelly, L. E. it, ~ L. Was 1986 ~- ~ ad n~- moat gag 10,~9 bats. ~ ^ gaff MICA 76~8~85. ~ rm,~. 1986 P~gY ~ ~e Act. a. ~1~20 ~ T. Old, a., ~ ~a f = ~ asps ad Get. ~ : W. B. ~en. ~CL~ 1986 Pawn ~ plea 1~ ~ Bat ~e ~ mats. Oat O~ ~- ~y 29:835~9. Ge~s,^.T. 1987 ~ Ate fig ad _ ma ~ ~e use ~es. Beat Dev~ev~~ 13:2~9. Haaga, 1. G. 1986 We Accra ~R~-c~e Dan ~ ~ Music may ~ Say, Ch. X, N-2157-~, `u ala, CA: we ~ Dada. 1987 Pa d_ ~ ~ it: ad_ a As For plagues. ^~^ 12:1~1~. __ 1987 Vat ~ =~ no_ m-- For dot as ~ gal multi. ~ ^~ Of A~~y 73 :~3. H~,J.P.,R.~a~-,C.Ya~,R.~.~=dR.E.~e~ 1~4 H~~ ad w6~" a^ ~p~- At: How ~ ~ tic Yes ~ gal _?" ~ ~' 1 :611~15. ~,1~ 1986 Odes mamma age ~ pa ala: s get ~ ~ Hmmmm. a ~ ~~ S~ 41 :7~42. Ha~s-, K. A. 1985 Dig, ~ ad sag plots: ~ sag ~ 22,~4 asset= Has norm Gaff. B,Z'~A Oaf ~= ~ ~- 9~.):1~2. 1~9 ~ ~ Id s==ss~ ~ Marcy. I. 41 44 ~ P=--ed~ HI -~=d-, ^~~ ~= ~^g Hum= ~_~c Safe=. 185. Isle= D.C.: Pa ^~ HI it. Ha, E. B. 1985 ~ ~e, ammo age, ad ~= Posse Act: namm, mag~mde, _ Orgy, ~ me~sm ~ I. Bag [~ ~~ 36:117-132. 1986 bat Isis of ~ ad Id ~ ~ Java ~ Bag. ^ Bi=~' ~. 18~-118. s~ ~ redate ~l ~ ~ Smog He Vat ~ ~ B-w~[ 1985 F~ve~~g a. Cast-, D.C.: ^~ Away pass.

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~36 lOHNG.HMGA Kane,S.H. 1967 Advancing age and the primigravida. Obstetrics and Gynecology 29:4~14. Kessel, E., S. Sastrinawata, and S. D. Mumford 1985 Correlates of fetal growth and survival. Acta Pacdiatrica Scandinavia 3 19(Suppl.): 12~127. Kielmann, A., and associates 1983 Child and maternal health services in nual Iddia: the Narangwal c~penment. Integrated Nutrition and Child Care, Vol. 1. Baltimore, Md.: Johns Hopkins University Press. Kiely, J. L., N. Pameth, and M. Susser 1986 An assessment of the effects of maternal age and parity in different components of perinatal modality. American Jown~1 of Epidemiology 123:411 454. Klebanoff, M. A. 1988 Short inte~pregnancy interval and the risk of low bi~thweight. American Journal of Public Health 78:667~70. Kramer, M. S. 1987 Intrauterine growth and gestabonal age detcrnunants. Pediatrics 80:502-511. Lawrence, M., W. A. Coward, F. Lawrence, T. Cole, and R. Whitehead 1987 Fat gain dunug pregnancy in rural African women: the effect of season and dietary status. American Journal of Clinical Nutrition 45:1442-1450. Lawson, J. B., and D. B. Stewart 1967 Obstetrics and Gynecology in the Tropics and Developing Countries. London: Edward Amold. McAnamey, E. R. 1987 Young maternal age and adverse neonatal outcome. American Journal of Diseases in Childhood 141:1053-1059. McGregor, I. A. 1984 Epidemiology, malaria, and pregnancy. American Journal of Tropical Medicine and Hygiene 33:517-525. Mehta, lo, and I. D. Young 1987 Recurrence risks for common complications of pregnancy. Obstetrical and Gynecological Survey 42:218-223. Millman, S. R., and E. C. Cooksey 1987 Birth weight and the effects of birth spacing and breastfeeding on infant mortality. Studies in Family Planning 18:202-212. Moja~ro, O., and R. Aznar 1986 ~fluencia de los factores biologicos y del estn~ctura social en la mortalidad infantil, 1965-74. Pp. 347-382 in J. Martinez Manautou, ea., Planificacion Familiar. Poblacion y Salud en el Mexico Rural. Mexico City: Instituto Mexicano del Seguro Social. Naeye, R. ~ 1981 Teenaged and pre-teenaged pregnancies: consequences of the fetal-matemal competition for nutnents. Pediatrics 67:1K150. 1983 Matemal age, obstetric canplicanons, and the outcome of pregnancy. Obstetrics and Gynecology 61(2):21(}216. Naeye, R. lo, N. Tafan, C. C. Marboe, and D. M. Judge 1977 Causes of pennatal modality in an African city. Bulletin of the World Health Organization 55:63-65. National Research Council, C=rlnittee on Maternal Nutntion 1970 Maternal Nutrition and the Course of Pregnancy. Washington, D.C.: National Academy of Sciences.

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INFANT HEALTH ~ 37 National Research Council, Committee on Nutntion of the Mother and the Preschool Child 1981 Nutrition Services in Pcrinatal Care. Washington D.C.: National Academy Press. Niswander, K. R. 1977 Obstetric factors Dated to pranatunty. Pp. 249-268 in D. W. Reed and F. J. Stanley, eds., Thc Epidemiology of Prematurity. Baltimore, Md.: U'ban and s~warzenbur Niswander, K. R., and M. Gordon 1972 Thc Women and Their Pregnancies: Thc Collaboratiw Pcrinatal Study of the National Institute of No urological Discascs and Strode. Philadelphia: W. B. Sanders. Ojo, A., and V. Omnsayc 1988 Who is the elderly pn''ugravida in Nigeria? International Journal of Gynaccology and Obstetrics 26:51-55. Overall, J. C. 1987 Vim1 infections of the fetus and recrate. Pp. 966 1007 in R D. Feigin and J. D. Cherry, eds, Textbook: Podiatric Infectious Discascs, 2nd ed. Philadelphia: W. B. Saunders. Pebley, A. R., and P. W. Stupp 1987 Reproductive patterns and child survival. International Family Planning Pcrspec- ti~cs 12(3):71-79. Peckham, C. S., C. Johnson, A. Ades, K. Pearl, and K S. Chin 1987 Early acquisition of cytomcgalo~us infection. Archives of Disease in Chidhood 62:780-785. Placek, P. 1977 Maternal and infant health factors associated with low infant birth weight: findings from the 1972 National Natality Survey. Pp. 197-212 in D. W. Reed and F. J. Stanley, ads., The Epidemiology of Prematurity. Baltimore, Md.: Urban and Schwarzenburg. Potter, J. E. 1988 Birth spacing and child survival: a cautionary note regarding the evidence from the WFS. Populatu~nStudics42(3)(Novembcr):443-450. Potter, J. E., O. Moiarro, and L. Nunez 1987 lbe influence of health care on contraceptive acceptance in rural Mexico. Studies At Family Planning 18:144 156. Powell~riner, E. 1987 Risk of Perinatal Death: A I^g-Linear Analysis of the Effects of Selected Factors on Pregnancy Outcome. Paper presented to the annual meeting of the Population Association of America, Chicago 111., May. Preston, S. H. 1985 Mortality in childhood: lessons from W.F.S. Pp. 253-272 in J. Cleland and J. HoLc~ft, eds., Reproductive Change in Developing Countries: Insights from the World Fcrtitity Surety. New Yodc: Oxford University Press. Puffer, R. R., and C. V. Serrano 1973 Pattems of Mortality In Childhood. PAHO Scientific Publication No. 262. Washington D.C.: Pan-Amcrican Health O~anizatian. 1975 Binhweight, Matemal Age, and Birch Order: Circe Important Detennunants in Infant Monality. PAHO Scicndfic Publication No. 294. Washington D.C.: Pan-American Health Organization. Rahman, M., B. Woityniak, and K. M. S. Aziz 1985 Impact of environmental sanitation and crowding on infant modality in Neal Bangladesh. The Lancet (Jelly 6):28-31.

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~38 lONNG.HAAGA Riley, L. W., S. H. Waterman, A. S. G. Faruque, and M. I. Huq 1987 Breast-feeding children in the household as a risk factor for cholera in rural Bangladesh: an hypothesis. Tropical and Geographic Medicine 39:9-14. Rosso, P., M. Wasserman, S. J. Rozowski, and E. Velasco 1976 Effects of matemal undernutrition on placental metabolism and function. Pp. 59 in D. S. Young and J. M. Hicks, eds, The Neonate. New York: Wiley. Royston, E. 1982 Prevalence of nutritional anemia in women in developing countries: a critical review of available information. World Health Statistics Quarterly 35:5~91. Santow, G., and M. D. Bracher 1984 Child death and time to next bid in central Java. Populatu~n Stu~lics 38(2)(July):241-253. Seeds, J. W. 1986 Malpresentations. Pp. 453~84 in S. G. Gabbe, J. Niebyl, and J. L. Simpson, ads., Obstetrics: Normal and Problem Pregnancies. New Yodc: Churchill Ii~ngstone. Seidman, D. S., R. Gale, P. E. Slater, P. Even-Hadani, and S. Harlap 1987 Does grand multiparty affect fetal outcome? International Journal of Gynaecology and Obstetrics 25:1-7. Sever, J. L., J. H. Ellenberg, and D. Edmonds 1977 Maternal Snaky tract infections and prematurity. Pp. 19~196 in D. W. Reed and F. J. Stanley, eds., The Epidemiology of Prematurity. Baltimore, Md.: Urban and Schwarzenburg. Smedman, L., G. Sterlcy, L Mellander, and S. Wall 1987 Anthropometry and subsequent mortality in groups of children aged 6-59 months in Guinea-Bissau. American Journal of Clinical Nutrition 46:369-373. Shield, J. P., and A. Galazka 1984 Neonatal tetanus in the world today. Bulletin of the WHO 62:647~69. Stanf~eld, S. K. 1987 Acute respiratory infections in the developing world: strategies for prevention, treatment, and control. Pediatric Infectious Diseases Journal 6:622-629. Strobino, D. M. 1987 The health and medical consequences of adolescent sexuality and pregnancy: a review of the literature. Pp. 93-126 in C. D. Hayes, ed. Risking the Future: Adolescent Sexuality, Pregnancy, and Childbearing? Vol. 2. National Academy of Sciences, Panel on Adolescent Pregnancy and Childbeanng. Washington D.C.: National Academy Press. Suskind, R. M., and M. Pariington 1981 Effects of postnatal malnutrition on the development of the immune response. Pp. 791-810 in E. Lebenthal, ea., Textbook of Gastrocntcrology and Nutrition in Infancy, Vol. 2. New York: Raven Press. Swanson, C. A., and J. C. King 1987 Zinc and pregnancy outcome. American Journal of Clinical Nutrition 46:763-771. Tsu, V. D., and N. Newton 1986 Appropnate technologies for pennatal care. Advances in International Maternal and Child Health 6:166 194. van den Berg, B. J., and F. W. Oechsli 1984 Prematurity. Pp. 69~5 in M. B. Bracken, ea., Perinatal Epidemiology. New York: Oxford University Press. Villar, J., and J. M. Belizan 1982 The relative contribution of prematurity and fetal growth mardaiion to low birth weight in developing and developed societies. American Journal of Obstetrics and Gynecology 143:793-798.

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INFANT HEALTH ~ 39 WHO Malana Action Programme 1987 World malaria situation 1985. World Health Statistics Quarterly 40(2):142-170. Winiclc, M. 1967 Cellular growth of human placenta. m. intrauterine growth failure. Journal of Pediatrics 71 :39(~395. Nutrition, intrauterine growth retardaiial, and the placenta. Trophoblast Research 1:71-84. World Health Organization 1987 Causes of infant death by sex and age, table xiv. World Health Statistics Annual, Genera, Switzerland. World Health Organization, Funnily Health Division 1981 Sununary of the ad hoc survey on infant and early childhood modality in Sierra Leone. World Health Statistics Quarterly 34:22~238. Wright, H. T. 1980 Cytomegalovirus infections. Pp. 17~172 in I. Last, ed, Maxcy-Rosenau Public Health am Preventive Medicine, 11th ed. New York: Appleton-Century-Crofts. 1983