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CHAPTER 2 Etiology and Risk Factors Despite important new research findings and improvements in the science of obstetr ics, our understanding of the basic causes of preterm labor and intrauterine growth retardation Is 1 imited . In the absence of adequate knowledge about etiology, a large body of information has developed about factors associated with low birthweight, often termed frisk factors, n because their an increased chance, or risk, of bearing a low b~rthweight infant. This chapter outlines data both on the etiology of prematurity and IUGR and on the risk factors associated with these outcomes of pregnancy. It also describes the process of risk assessment and analyzes several risk assessment systems. presence in an individual woman indicates Etiology As described in the previous chapter, the term low birthweight can refer to three often intertwined outcomes of pregnancy: preterm delivery, intrauterine fetal growth retardation (TUGR), and a combination of both. Although little is known about the various mechanisms that produce these conditions, several have been developed as a basis for further this section. ~ . Prematurity theoretical models research and are outlined in The mechanism for the initiation and maintenance of normal human labor is not known, but substantial progress has been made in understanding some of the important associated physiologic and biochemical events. ~ Information about the onset of preterm labor is more fragmentary and speculative. 2 Endocrine changes in the uteroplacental environment appear to be the principal factors leading to the development of uter ine contractions. 3 These endocrine changes involve hormones from both the mother and the fetus; cor tisol, estrogen, and progesterone appear to play ma jor roles . Much of this informal ion is based on stud ies o f sheep in which the process starts about 10 days before labor. 46

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47 The first event in sheep Is an elevation in fetal cortisol, probably in response to fetal ACTH. This cortisol rise generates a decline in maternal progesterone due to the induction of 17 a-hydroxylase enzyme activity in the placenta, which increases the conversion of progesterone to dehydroxyprogesterone. 4 Progesterone withdrawal is associated with increased uterine muscle excitability, or responsiveness to electrical and hormonal stimuli. Dehydroxyproges- terone also is a precursor of the rise in maternal estrogen, which occurs a few days before the onset of labor. Estrogens increase rhythmic uterine contractions and also the responsiveness of the uterus to oxytocin e In sheep, estrogen elevation also causes a rise in prostagland~n (PGF2a) production hours before the onset of uterine activity. The combined changes in maternal hormones are thought to affect uterine muscle by enhancing myometrial excitability and the conduction of action potential. In contrast to sheep, the human hormonal changes appear to occur during the last 5 weeks of pregnancy, and evidence for fetal cortisol initiating the onset of labor is lacking. Amniotic fluid cortisol and maternal blood estrogen increase at 34 to 36 weeks of gestation. The former correlates with fetal pulmonary maturity and the latter may play a role by increasing prostaglandin production. Unlike in sheep, the role of progesterone in human labor is unclear .3 A decline In peripheral blood levels before labor has been suggested in at least one study, 5 although others have failed to confirm this finding. The presence of a fetal membrane progesterone binding protein, possibly facilitated by estrogen, indicates that a local withdrawal effect may occur. Several reports indicate that prostaglandins do play a role in human labor; they are synthesized from a fatty acid precursor In the chorioamnion and/or decidua at a time when estrogen levels are increasing.6 7 Last, increased levels of maternal oxytocin are not thought to contribute to initiating labor (although a threshold level may be important as a permissive factor), but may be necessary for the development of more intense contractions during the second stage of labor. Fetal oxytocin may play a role, however, as indicated by high concentrations of this hormone in umbilical cord blood. The way in which hormonal changes act to induce labor Is not clear .2 3 Animal studies demonstrate that low resistance myometria1 pathways (gap junctions) form dur ing labor and suggest that the structural and biochemical organization of myometrial muscle may be important in the development of contractions. The development of gap junctions under the influence of steroids and prostagland~ns and in relation to the estrogen/progesterone ratio is probably of major importance to the organization of the myometrium.8 The contraction of uterine muscle is significantly influenced by an increase in the concentration of free calcium on the myofibrils resulting from the action of prostaglandins, which counteracts progesterone-~nduced calcium binding In the sarcoplasm~c reticulum. Knowledge about the etiology, initiation, and maintenance of preterm labor is limited. 2 9 A The underlying pathophysiology is postulated on the basis of variations from the normal patterns of hormonal effects detected in animals and man or on the basis of -

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48 inferences made about the possible untoward effects of certain clinical conditions on uteroplacental physiology. Observations suggest that infection, stress, hypertension, and other conditions may be associated with variations in the endocrine environment and metabolic state of the uterus and the cervix. These variations probably result from complex interactions involving progesterone, estrogen, oxytoc in, and other hormones; prostaglandins; calcium ions; adrenergic agents and receptors; catecholamines; and~uteroplacental blood flow. From the foregoing, it is clear that at this time it is not possible to identify a single etiology for premature birth.2 It is possible, however, to enumerate a variety of factors and clinical conditions that have been associated with the preterm onset of labor. This list includes, but is not limited to, abruptio placentae, amnionitis, congenital malformations, erythroblastosis fetalis, incompetent cervix, placenta previa, polyhydramnios, preeclampsia, premature rupture of membranes, severe maternal illness, multiple pregnancies, and urinary tract infections. In general, these are conditions in which there is an inability of the uterus to retain the fetus, interference with the course of the pregnancy, premature separation of the placenta, or a stimulus to effective uterine contractions before term. Several of these conditions are discussed later in the chapter as risk factors for preterm birth, although it is apparent that the distinction between a r isk factor and a causal mechanism is not always clear. Finally, in many cases of premature birth, no association with a pathologic factor can be identified. _ Intrauterine Growth Retardation (IUGR) Delay in the growth and development of the fetus has been associated with a variety of factors that can be grouped in terms of the locus of their impact: the placenta, the pregnant woman herself, the fetus, or some combination of these. In general, IUGR is associated with conditions that interfere with the circulation to and efficiency of the placenta, with the development or growth of the fetus, or with the general health and nutrition of the pregnant woman; however, for many growth-retarded infants no relevant pathogenic factors can be identified. Vascular and inf lammatory lesions of the placenta; placental separation and infarction; and decreases in placental weight, cellularity, and surface area may act alone or in combination to produce TUGR.~ It is postulated that such conditions result directly or indirectly in a reduction in the supply of nutrients to the fetus. 12 Multiple pregnancies (for example, twins or triplets) also may be associated with IUGR because the placenta may be unable to supply sufficient nutrients to multiple fetuses. Other placental conditions associated with IUGR include hemangioma of the placenta or umbilical cord and the parabiotic transfusion syndrome. Insufficient placental transfer of nutrients may be primarily related to abnormal transport across the placenta, to alterations in placental metabolism, or to changes in the uteroplacental circulation. 3

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49 Certain conditions or diseases of pregnant women also are associated with IUGRe ~ 4 ~ 5 They are thought to directly or indirectly hamper delivery of nutrients or oxygen to the uteroplacental circulation, which results in an inability to maintain normal fetal growth and development. 6 The most frequent, recognized problem Is the presence of a maternal vascular disease, such as chronic hyper- tension or chronic renal disease. The duration and severity of the ~ . . ~ . . . ~ absorber are roughly refaced co One severity of the IUGR. Pregnancy- induced hypertension also can cause IUGR, but commonly the fetus is delivered before severe growth retardation develops. This condition, super imposed on chronic hypertension, often is associated either with IUGB or premature delivery of a fetus that has grown and developed normally up to the time of delivery. Severe forms of diabetes mellitus _ . . . ~ . , also are frequently associated with vascular disease and IOGR. Sickle- cell disease may be associated with IUGR and placental lesions. Several conditions that lead to hypoxia in pregnant women have been associated with IUGR, including cyanotic heart or pulmonary disease and residence at high altitudes. 6 ~ 7 A variety of mechanisms have been postulated for the development of IUGR associated with cigarette smoking, alcohol and narcotic ingestion, and the administration of antimetabolites, but no definitive statement can be made concerning these etiologies. Similarly, the precise pathogenic mechanisms linking maternal malnutr ition and chronic illness during pregnancy to low birthweight (IUGR or prematurity) are unknown. Fetal factors implicated by association in the etiology of IUGR include chromosomal disorders, such as certain autosomal trisom~es; chronic fetal infections, such as congenital rubella, syphilis, and cytomegalovirus inclusion disease; certain congenital malformations and diseases; and radiation injury. ~8 Although a variety of pathogenic mechanisms have been suggested by these associations, the specific etiologies have not been established conclusively.~5 Finally, TUGR and prematurity occur together in about 30 percent of low birthweight cases. In some instances, both the prematur ity and the IUGR occur without a demonstrable association with a suspected pathogenic factor. In other cases, various combinations of the factors discussed above can be identified. Risk Factors: An Overview Recent research on the risk factors associated both with preterm delivery and TUGR has helped to identify possible causes of low b~rthwe~ght. Risk factor analysis also helps guide clinical practice and suggests possible prevention strategies at both the individual and population level. Unfortunately, the risk factor literature has many methodological and conceptual problems that make its interpretation cliff icult. For example, many studies analyze the relationship of a given risk factor to slow birthweight" rather than to the more specific outcomes of preterm delivery and intrauterine growth retardation; also, these studies commonly rely on estimates of gestational age, which often are

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so approximate. Risk factors often are defined differently in different studies, and studies of small groups often do not produce information that can be applied to other populations, thereby hampering comparisons and pooling of data. More importantly, many studies examine risk factors as independent entities, although several factors may cluster in an individual and may be causally related. Finally, known confound- ing variables may not be controlled, and the cross-sectional design of many r isk factor studies makes it cliff icult to separate cause and effect. Such problems make it hard to reach conclusions about the magnitude of risk posed by single factors. Some of these limitations can be overcome by more careful statis- tical design and definition. Others are more difficult to correct. For example, many population-based studies must rely on data derived from birth certificates; in most states, these forms include only a limited number of risk factor variables relevant to low birthweight. Birth certificates in most states do not provide information on such factors as maternal height, weight, weight gain during pregnancy, or smok ing practices . A chart listing the principal risk factors for low birthweight is shown in Appendix A. Based on the studies noted in the appendix, in this chapter, and in Chapter 3, the chart records whether a given factor has been reported to increase the risk of preterm delivery or IUGR, or whether it has simply been linked to low birthweight. For some factor s, the char t also records attr ibutable and relative r isk values (defined In Chapter 11. Appendix A includes a mixture of factors for which the evidence of risk is strong and those for which the association with prematurity and/or IUGR is less clear. Because some studies have calculated relative or attributable risk values for certain factors , the committee explored the possibility of ranking the risks in order of magnitude to help set priorities for interventions and for further research. Unfortunately, the data do not permit such ordering. For some factors (including many of the infections), the committee was able to locate no risk values at all For many others, only a single value was located, and the committee judged this to be an inadequate data base from which to construct a ranking of magnitude of r isk . Another problem is that r isks imE,or ten t at an individual level are not always so for populations. It is also apparent that the estimates of risk vary significantly, probably due to def initional var. Cations and to differences in populations studied. The committee also concluded that, because of the numerous interrelation- ships among factors, it would be unwise to address them in a way that suggests each always has an independent influence on preterm delivery or IUGR. Even without an orderly ranking of risk, the committee found that the factors could be grouped in a way that helps to structure preventive interventions, which is the pr incipal focus of the repor t. In Table 2.1, which summarizes Appendix A, the risk factors are separated into demographic characteristics, medical risks that can be detected before conception, risks that can be detected during pregnancy, behavioral and environmental r isks, health care r isks, and a final category of factors whose role in low birthweight is still being def ined.

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51 TABLE 2.1 Principal Risk Factors for Low Birthweight I. Demographic Risks A. Age (less than 17; over 34) B. Race (black) C. Low socioeconomic status D. Unmarried E. Low level of education II. Medical Risks Predating Pregnancy A. Parity (D or more than 4) B. Low weight for height C. Genitourinary anomalies/surgery O. Selected diseases such as diabetes, chronic hypertension E. Nonimmune status for selected infections such as rubella Poor obstetric history, including previous low birthwe~ght infant, multiple spontaneous abortions Maternal genetic factors (such as low maternal weight at own birth) III. Medical Risks in Current Pregnancy A. Multiple pregnancy B. Poor weight gain C. Short interpregnancy interval D. Hypotension E. Hypertension/preeclampsia/toxemia F. Selected infections such as symptomatic bacteriuria, rubella, and cytomegalovirus G. First or second trimester bleeding H. Placental problems such as placenta previa, abruptio placentae I. Hyperemesis J. Oligohydramnios/polyhydramnios R. Anemia/abnormal hemoglobin L. Iso~mmunization M. Fetal anomalies F. G. N. Incompetent cervix 0. Spontaneous premature rupture of membranes IV. V. Behavioral and Environmental Risks A. Smoking B. Poor nutritional status C. Alcohol and other substance abuse D. DES exposure and other toxic exposures, including occupa- tional hazards E. High altitude Health Care Risks A. Absent or inadequate prenatal care B. Iatrogenic prematurity VI. Evolving Concepts of Risk A. B. C. Stress, physical and psychosocial Uterine irritability Events triggering uterine contractions D. Cervical changes detected before onset of labor E. Selected infections such mycoplasma and Chlamydia trachomatis F. Inadequate plasma volume expansion G. Progesterone deficiency This grouping leads to the observation that many of the risk factors for low birthweight (categories I, II, and IV of the table) can be identified before pregnancy occurs; detection and possible intervention need not always wait until the prenatal per iod . Chapter 5 develops this theme more fully. The grouping also helps to highlight the importance of behavioral and environmental risks anu one neec~ tor interventions that go beyond medical care. The demographic measures can help to define target populations. The cluster of health care issues highlights the fact that not all r isks for low birthweight ~ ~ . _ -

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~2 derive from characteristics of women themselves. And finally, the category of evolving concepts of risk suggests some important research areas for improved understanding of low birthweight. These themes appear throughout Part lI of this report. In the following detailed discussion of risk factors, the committee chose to focus on those that are widely distr ibuted throughout the population, amenable to prevention or treatment, or especially controversial. These include the demographic risk factors of race, age, and socioeconomic status; the medical and obstetr ic r Asks of hypertension/preeclampsia, diabetes, obstetric history (including previous induced abortion), multiple pregnancy, and infection; nutr ition; the behav ~ oral and environmental r isks of smok ing and alcohol use; and iatrogenic prematur ity. The committee also examines certain r isk factors that are more speculative in nature, including stress, uterine irritability, cervical changes, inadequate plasma volume expansion, and progesterone deficiency. Chapter 3, a review of state and national vital statistics data, provides additional information on some of the demographic factors and on the issues of pregnancy interval, obstetr ic history, and parity in relation to age. Chapter 6 explores another risk factor for low birthweight, absent or inadequate prenatal care. Demographic Risks The interrelationships among the major demographic risk factors are numerous and it is often difficult to determine the precise association between any single factor and low birthweight . Nonetheless , through careful statistical design, the independent effect of each is gradually be ing def ined . Race Table 2.2 shows the frequency of low birthweight for different racial and ethnic groups. The approximate 2:1 low birthweight ratio between black and nonblack ethnic groups has remained fairly constant for the past 20 years. When ~ ow birthweight infants are subdivided into those born at term and those born prematurely, blacks remain approximately twice as likely as whites to be in either category.~9 In one large but now dated study of approximately 50,000 pregnancies, black newborns were on average 233 grams lighter than the' r white counterparts .2 0 That black neonates are at high risk of low b~rthweight is unquestioned. The reason or reasons for this r isk are uncertain, however. Maternal age may account for part of the increased r isk. Teenage mashers are at high risk of low b~rthweight, and black mother are more likely to be teenagers than are mothers of other ethnic groups. In 1980, 26.5 percent of all black births were to teenagers. In contrast, 12.1 percent of white births and 15.3 percent of Hispani births were to teenagers. When black and white mothers of the same . s ic

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53 TABLE 2.2 Percentage of Live Births Less Than 2,500 Grams Percent Less Than 2,500 Grams Percent Less Than 1,500 Grams White 5~7a 0.9a Black 12.5a 2.4a Chinese 4.9a o.6a Mexican-American S.3b o.9b American Indian 6.9c -- SOURCES: aNational Center for Health Statistics: Characteristics of Asian Births: United States, 1980. Prepared by S Taffel. Monthly Vital Statistics Report, Vol. 32, No. 10 (supplement). Public Health ~ Washington, D.C. : U.S. Government Printing Office, February 1984 . National Center for Health Statistics: Births of Hispanic Parentage, 1979. Prepared by SJ Ventura. Monthly Vital Statistics Report, Vol. 31, No. 2 (supplement). Public Health Service. Washington, D.C.: U.S. Government Printing Office, May 1982. CNational Center for Health Statistics: Factors Associated with Low Birthweight, 1976 . - ~ - ~ ~ ~ -- ~ ~ ~ - ~ ~ - ~ ~ ~ Series 21, No. 37. Prepared by S Taftel. Vital and Health Statistics, DHEW No. (PHS) 80-1915. Public Health Service. Washington, D.C.: U.S. Government Printing Office, April 1980. age are compared, however, blacks are at higher risk of low birthweight in every age group.22 The relationship of low birthweight to maternal age using 1976 data is shown in Table 2 .3; Appendix Table B.7 displays more recent and more detailed data on the same subject. Low level of maternal education is another r isk factor for low birthweight and is often used as a proxy for socioeconomic status. Table 2.4 shows the relationship between race, education, and low birthweight. In general, black mothers are less educated than white mothers. In 1980, 35 percent of black women who delivered live-born babies had completed less than 12 years of school, versus 20 percent of whites. At the other end of the educational spectrum, 16 percent of white mothers and 6 percent of black mothers were college graduates.2i Educational differences do not account for the racial differences in low birthweight, however. When matched for both age and education, blacks are still at higher risk of low birthweight.22 See also Appendix Table B.9. Black women are more likely than white women to delay initiation of prenatal care.2 ~ However, when receipt of prenatal care is held constant, black women are still at increased risk of delivering a low birthweight baby.2 3 A limitation of most studies in this area is the

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54 TABLE 2.3 Maternal Age and Percentage of Infants Less Than 2,500 Grams, 1976 Maternal Age (year s) ite Black {percent) (percent) Less than 15 11.8 17 .1 15-19 8.1 14.7 20-24 6.0 12.6 25-29 . 5 .3 11.3 1 30-34 5.8 11.6 35-39 7.0 13.1 40-44 8.3 12.8 45 49 9.4 16.3 SOURCE: National Center for Health Statistics: Factors Associated with Low Birthweight, 1976. Prepared by S Taffel. Vital and Health Statistics, Series 21, No. 37. DHEW No. (PHS) 80-lgl5. Public Health Service. Washington, D.C.: U.S. Government Printing Office, April 1980. inability to adjust for the quality or content of prenatal care received. Chapter 6 takes up this issue in detail. To control for the effects of other variables that may be related to race, such as maternal stature, smoking, and others that are not included on birth certificates, one can look at special studies, such as the Collaborative Perinatal Study, which, though dated, remains an important and detailed survey of a number of important issues and processes in pregnancy. At the time of that project, fewer black than white women smoked, and among the smokers, white women smoked more than black women. When smoking status was controlled, blacks were still twice as likely as whites to have low birthweight infants. The height distributions of blacks and whites were almost identical, while blacks tended toward slightly higher prepregnant weights. At almost every combination of height and weight, and for almost every combination of weight and weight gain, black women were at hither risk of low birthweight Than white women. Furthermore, black women were at higher risk of low birthweight at all combinations of age and parity.20 Finally, it has been shown that women whose last infant was of low birthweight are at increased risk of low birthweight in the current pregnancy.24 Yet in the Collaborative Study, when women were stratified by whether or not their last child was low birthweight, blacks were still at increased risk of low birthweight during the

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55 TABLE 2.4 Percentage of Single Live Births Less Than 2,500 Grams by Race and Educational Attainment of Mother White Maternal Educational Atta inment (year s ~ 1972 1977 (percent) (percent) Black 1972 1977 (percent) (percent) Less than 12 7 .29 6 .99 13 .59 13 .04 12 5.16 4.74 10.85 10.31 13-15 4.43 4 .09 9.76 9.41 16 or more 3.97 3.63 8.92 8.15 NOTE: Adjusted for maternal age and total birth order. Women under age 20 excluded. SOURCE: National Center for Health Statistics: Trends and variations in birth weight. Prepared by JC Rleinman. In Bealth, United States, 1981, pp. 7-13. DHHS No. (PHS) 82-1232. Public Health Service. D.C.: U.S. Government Printing Office, 1981. Washington, current pregnancy.2 In sugary, anthropometric and obstetric differences do not appear to account for the increased r isk of low birthweight seen in blacks. In trying to understand the nature of this r ask factor, it is worthwhile to examine the low birthweight incidence among Mexican- Americans, who are economically and sociodemographically similar in some respects to black Americans, yet have been reported to have a very low incidence of low b~rthweight. In 1979, 5.3 percent of Mexican- , . _ Amer ican newborns weighed less than 2 , 500 grams, compared with 5.7 percent of white babies and 12.8 percent of black babies.2 ~ This low incidence among Mexican-Amer loans is not readily explained. I t may be due in part to problems in data reporting. Selby et al. recently showed, for example, that the Spanish surname infant mortality rate may appear lower than it actually is because of uneven reporting of infant mortality in this population and that it is therefore an inaccurate indicator of Mexican-American health status.2s Similar data problems may skew reporting of low birthweight. The large difference between black and Mexican-American low b~rthweight rates also raises the possibili ty that cultural differences may play a role in pregnancy outcome. The very low incidence of childbear ing among unmarr fed Mexican-Amer ican women, unlike that among black women, and their different dietary practices and family structures support this notion. The forthcoming Hispanic HANES surrey should provide information on the physical stature and health-related behavior of Mexi-can-Amer icans and perhaps help to clarify the reasons for the low rate of low birt}1weight observed in Mexican-ATner~cans.

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56 The issue of race and low birthweight is further complicated by the different birthweight-specif~c neonatal mortality rates of white and black infants that have been noted in a variety of populations. Black infants born at less than 2,500 grams have long been recognized to have better rates of survival in the neonatal period than low birthweight white infants of similar birthweights.2 6 2 7 The conclusion to be drawn from the complicated data on race, low birthweight, and race- and birthweight-specific mortality is that the reasons for the risk differential between white and black neonates are not well understood. The cumulative effects over time of poverty and social neglect, and the interaction of such factors with biological parameters, undoubtedly have played a role In these racial differences; other factors remain to be defined. Research should be pursued to obtain a better understanding of these issues. Age U. S. vital statistics data show that in 1978, 17 percent of all births were to teenagers, yet 24 percent of all low birthweight infants had a teenage mother.28 The relationship of low birthweight to age was shown in Table 2.3 The rate for both whites and blacks is highest at very young ages. It falls throughout the teenage years and reaches its lowest point between 25 and 29 years. Thereafter, the low birthweight rate rises slowly with increasing maternal age. Teenage mothers, particularly the youngest (under age 15), have many other risk factors that could be responsible for an adverse pregnancy outcome. First births are more likely than later births to be low-weight, and young mothers are more likely to be having their first birth. However, when only first births are examined' teenagers are still at higher risk than older mothers.22 Very young teenagers having higher-order births are a particularly higher isk group, probably in part because such births imply a short interval between pregnancies, which itself Is a risk factor for low birthweight. Thirty percent of second- and higher-order births to women less than 15 in 1978 were low b~rthweight. Fortunately, there were fewer than 350 such births in the United States in 1978. Young mothers are more likely to be black and of low socioeconomic status, to report late for prenatal care, and to be unmarrzed.28 They tend to be shorter and lighter than their older counterparts.29 Young teenagers, not being old enough to have completed their school- ing, are less educated than older women. These factors in combination appear to account for the higher rate of low birthwe~ght in teenage mothers. For example, in one study, 422 consecutive prim~gravidas less than 16 years old delivering at a hospital were matched by race to 422 primigrav~das aged 20 to 24 delivering at the same hospital. The adolescent mothers delivered infants that were 40 grams lighter on average than the young adult mothers, but the difference was not statistically significant. It was noted that the adolescents were more likely to be clinic patients, unmarried, and live In a census tract with low buying power. They were shorter and lighter as well. When

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83 intervention. Important ones listed at the beginning of the chapter include several sociodemographic factors; various medical and obstetric risks; certain behavioral, environmental, and occupational factors; and selected risks based in health care practices. It Is also apparent that risks for low birthweight are widely distributed throughout the population and that a substantial amount of low birthweight will continue to occur outside of groups defined as high risk. This fact highlights the need for greater understanding of r isk and etiology; it should not be used to minimize the value of using existing r isk information for targeting interventions. Risk factor data also suggest another conclusion. Many of the established risk factors are amenable to prevention or therapy, and of these, many can be recognized before pregnancy occurs. Smoking Is perhaps the best example. Other examples include poor nutr itional status, certain chronic illnesses, and susceptibility to infections such as rubella. Even demographic risk factors such as age can be managed before conception, for instance, by avoiding pregnancy at extremes of the reproductive age span; and the risks posed by high parity and brief interval between pregnancies can be decreased through family planning. Another major conclusion that emerges from the literature on the to answer very long list of questions. Our understanding of the basic causes of preterm labor and IUGR is seriously inadequate. A 1983 workshop sponsored by the National Institute of Child Health and Human Developments 6 ~ outlined promising research areas pertinent to IUGR, and a recent review article by Huezar and Naftolint touches on a etiology of low birthweight is that more research is needed number of topics that should be studied to provide a better under- standing of the normal onset of labor and of the pathogenesis and process of preterm labor. In the absence of more complete information about basic causal mechanisms, efforts to prevent low birthweight will remain ~ zmited. Factors whose role in low birthweight are uncertain need additional analys is . Stress, for example, may be a s ignif icant r isk factor for both IU=R and preterm labor, but more research is needed to understand the nature and magnitude of this risk. Other possibilities that merit study include, for example, the role of selected genitour inary infections in low birthweight, the natural history of uterine activity throughout pregnancy (to determine the value of uterine activity assessment as an index in evaluating the risk of preterm labor), and related topics mentioned in the section on evolving concepts of risk. Well-established risk factors also require more attention. For some factors, such as race, research is needed to understand why the risk exerts its effect. For others, such as alcohol, the magnitude of risk at various levels of consumption needs to be better defined. For both known and less-certain r isk factors, efforts should be made to distinguish risks for very low birthweight (1,500 grams or less) from risks for moderately low birthweight (1,500 to 2,500 grams) at various gestational ages. As Chapter 3 suggests, the incidence trends and sequelae of these two classes of low birthweight differ. Relating individual r isk factors to more ref. ined measures of low birthweight should provide clues to both cause and prevention.

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84 The committee's review of r isk assessment systems and instruments suggests that they are helpful in distinguishing between h ~ gh- and low-risk women. The significant incidence of low birthweight deliveries in low-risk individuals and groups suggests, however, that additional research is needed to improve the predictive capabil ity of these systems. It also indicates that clinicians must be alert to the possibility of low birthweight even in pregnant women judged to be at low r isk of such an outcome. Refer ences 1. Husaar G and Naftolin F: The myometrium and uterine cervix in normal and preterm labor . N . Engl . J . Med . 311: 571-581, 1984 . 2 . Bar den TP: Premature labor. In Neonatal-Perinatal Medicine, edited by AA Fanaroff and RJ Martins, pp. 139-144. St. Louis: The C.V. Mosby Co., 1983. 3. Speroff L, Glass RH, and Rase NG, eds.: Clinical Gynecologic Endocrinology and Infertility, 3rd Edition, pp. 316-322. Baltimore/London: Williams and Wilkins, 1983. 4. Liggins GC: Premature delivery of foetal lambs infused with ghicocorticoids. J. Endocr inol. 45: 515-523, 1969 . 5. Turnbull AC, Flint APE, Jeremy JY, Patten PT, verse MJNC, and Anderson ABM: Significant fall in progesterone and rise in estradiol levels in human peripheral plasma before onset of labour . Lancet I :101-104, 1974 . 6. Nosy ~ and Liggins GC: Role of prostaglandins, prostacyclin and thromboxanes in the physiologic control of the uterus and in per tur ition. Seminar Perinatol. 4:45-66, 1980. 7. Challis JRG and Mitchell F: Hormonal control of preterm and term partur itzon. Seminar Perinatol. S: 192-202, 1981. 8. Car sten ME: Calcium accumulation by human uterine microsomal preparations: Effects of progesterone and ocytocin. Am. J. Obstet. Gynecol. 133:598-601, 1979. 9. Tamby Raja RL, Anderson ABM, and Turnbull AC: Endocrine changes in premature labor. Br. Med. J. 4:67-71, 1974. 10. Cr easy RR and Liggins GC: Actiology and management of preterm labour. In Recent Advances in Obstetrics and Gynecology edited by J Stallworthy and GG Bourne, pp. 21-45. Edinburg: Churchill L ivingstone, 1979 . 11. Shanklin DR: Influence of placental lesions on newborn infants. Pediatr. Clin. North Am. 17.25-42, 1970. 12. Gruenwald P: Chronic fetal distress and placental insufficiency. Biol. Neonat. 5: 215-265, 1963. 13. Scott RE and Usher R: Fetal malnutr ition: Its incidence, causes and effects. Am. J. Obstet. Gynecol. 94:951-963, 1966. 14. Hobel CJ: Prevention of preterm delivery. In Fetal Physiology and Medicine, edited by RW Beard and PW Nathaniels, pp. 757-779. New York: Marcel Dekker, 1984. 15. Rliegman R and Rins K: Intrauterine growth retardation: Determinants of aberrant fetal growth. In Neonatal-Per inatal

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85 Medicine, edited by AA Fanaroff and RJ Martins, pp. 49-80. St. Louis: C.V. Mosby, 1983. 16. Behrman RE and Kliegman R: The fetus and the neonatal infant. In Nelson Textbook of Pediatrics, edited by RE Behrman and VC Vaughan III. 12th Edition, pp. 322-416. Philadelphia: W.B. Saunders, 1983 . 7. Siegel LS: Reproductive, perinatal, and environmental variables as predictors of development of preterm {less than 1501 grams) and fullterm children at 5 years. Semin. Perinatol. 6:274-279, 1982 ~ 18. Davies DO: Growth of "small for dates" babies. Early Hum. Devel. 5: 95-104, 1981. 19. Ressel SS, Villar J. Berendes HW, and Nugent RP: The changing the United States: 1970-1980. 24. 25. 26. J. Ber endes pattern of low birth weight in JAMA, 251: 1978-1982, 1984. 2 0 . Niswander KR and Gordon M: The Women and Their Pregnancies: The Collaborative Per inatal Study of the National Institute of Neurologic Diseases and Stroke. Philadelphia: W.B. Saunders Company, 1972 . 21. National Cente~ for Health Statistics: Births of H~spanic Parentage, 1979. Prepared by SJ Ventura. Monthly Vital Statistics Report, Vol. 31, No. 2 (supplement). Public Health Service. Washington, D.C.: U.S. Government Printing Office, May 1982 . National Center for Health Statistics: Factors Associated with Low Birth Weight: United States, 1976. Prepared by S Taffel. Vital and Health Statistics, Series 21, No. 37. DHEW No. (PHS) 80-1915 . Public Health Service . Washington, D.C.: U. S . Government Pr inting Off ice, Apr il 1980 . 23 . Mar k Klebanof f, Epidemiology and Biometry Research Program , National Institute of Child Health and Human Development, Bethesda, Md. Personal communication, 1984, based on an analysis of 1977-1981 birth certificate data from Baltimore, Maryland, and on the 1974-1977 Northern California Kaiser-Permanente Birth Defects Study. Bakketeig LS, Hoffman HJ, and Harley EE: The tendency to repeat gestatzonal age and birth weight in successive births. Am. J. Obstet. Gynecol. 135:1086-1103, 1979. Selby ML, Lee ES, Tuttle DM, and Loe HO Jr: Val~dity of the Spanish surn~me infant-mortality rate as a health status indicator for the Mexican Amer ican population. Am. J. Public Health 74:988-1002, 1984. W~lliams RL: Measuring the effectiveness of perinatal medical care. Med. Care ~ 7: 95-110, 1979. 27. North AF and MacDonald KIM: Why are neonatal mortality rates lower in small black infants than in wh ite infants of s zmilar b~rthweight? J. Pediatr . 90: 809-810, 1977. 28. National Center for Health Statistics: Vital Stat~stics of the United States, 1978 . Vol. I . DHHS No. (PHS) 82-1100 . Public Health Service. Washington, D.C .: U. S. Government Pr inting Office, 1982.

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