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Gestational Cocaine Exposure and Intrauterine Growth: Maternal Lifestyle Study

From The University of Kentucky, Lexington, Kentucky; Research Triangle Institute, Research Triangle Park, North Carolina; University of Miami, Miami, Florida; Wayne State University, Detroit, Michigan; Brown University, Providence, Rhode Island; National Institute of Child Health and Human Development, Bethesda, Maryland; George Washington University, Washington, DC; National Institute on Drug Abuse, Bethesda, Maryland; Center for Substance Abuse Treatment, Rockville, Maryland; and Administration for Children, Youth and Families, Washington, DC.

Address reprint requests to: Henrietta S. Bada, MD, MPH, University of Kentucky Chandler Medical Center, Department of Pediatrics, Room MS-473, 800 Rose Street, Lexington, KY 40536; E-mail: hbada2{at}uky.edu.

	ABSTRACT

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OBJECTIVE: To estimate the effects of cocaine exposure on intrauterine growth and to investigate at what point in gestation growth deviation would be manifested.

METHODS: This is a secondary analysis of data from a multicenter project, the Maternal Lifestyle Study, designed to determine infant outcomes of in utero cocaine or opiates exposure. Four centers of the National Institute of Child Health and Human Development Neonatal Research Network enrolled 11,811 maternal–infant dyads. A total of 1072 infants were cocaine exposed, 7565 were cocaine negative by maternal history and meconium results, and 3174 were excluded from analysis because of unconfirmed negative exposure. Outcome measures included birth weight, length, and head circumference.

RESULTS: Percentile estimates for birth weight, length, and head circumference revealed growth deceleration in cocaine-exposed infants evident after 32 weeks’ gestation. There was significant interaction between cocaine and gestational age. After controlling for confounders, at 40 weeks’ gestation, cocaine exposure was estimated to be associated with a decrease of 151 g, 0.71 cm, and 0.43 cm in birth weight, length, and head circumference, respectively. Smoking had a negative impact on all growth measurements, with some indication of a dose–effect relationship. Heavy alcohol use was associated with decrease in weight and length only. Opiates had significant effect only on birth weight.

CONCLUSION: In utero cocaine exposure is associated with growth deceleration involving all measurements, becoming more pronounced with advancing gestation.

From the 1999 and 2000 National Household Survey on Drug Abuse, the annual rates of current use of illicit drugs, tobacco, and alcohol were 7.5%, 30.3%, and 47.2%, respectively,¹ among women 15–44 years old. Of those women who were pregnant in the same age group, 3.3%, 19%, and 12.4%, respectively, used illicit drugs, tobacco, and alcohol, indicating that a large number of women continued their substance use during pregnancy. In the United States in 2000, there were 4,063,000 births to women aged 15–44 years.² Using estimates of substance use during pregnancy, the approximate numbers of births in 2000 complicated by maternal use of illicit drugs, tobacco, and alcohol were 134,079, 774,814, and 503,812, respectively. Thus, from the public health perspective, the impact of substance use during pregnancy extends far beyond maternal health to that of a large number of the unborn population.

Intrauterine growth restriction has been reported in infants born to drug-abusing mothers. Described manifestations of growth restriction in gestational cocaine exposure included lower birth weight, smaller head circumference, and decrease in birth length,^3–5 and in some studies, only one or two of these parameters were affected.^6–8 Reverse pattern of asymmetric growth restriction,^9,10 wherein head circumference is decreased relative to birth weight, has also been described. Furthermore, it is not clear at what point in gestation or fetal life does growth deviation or deceleration become evident. Effects of drug exposure on growth are also difficult to assess because of confounding effects of other factors, such as alcohol, tobacco, marijuana, and maternal medical and obstetric complications.^4,5,11 The objective of this study was to characterize intrauterine growth associated with in utero exposure to cocaine, in a large population recruited and being evaluated prospectively as part of a multicenter collaborative effort, the Maternal Lifestyle Study.^12,13 A large study population has the potential for investigating not only effects of cocaine exposure on growth but also of other factors. We hypothesized that deviation in growth associated with in utero cocaine exposure would be evident at each week of gestation throughout pregnancy, independent of the effects of other factors, including maternal use of other substances, such as opiates, alcohol, tobacco, and or marijuana.

	MATERIALS AND METHODS

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The Maternal Lifestyle Study is conducted in four centers of the National Institute of Child Health and Human Development Neonatal Research Network. These centers include Brown University, Providence, RI; University of Miami, Miami, FL; The University of Tennessee, Memphis, TN; and Wayne State University, Detroit, MI. The Research Triangle Institute, Research Triangle Park, NC, serves as a data coordinating center, a role assumed in the early phase of the study by the Biostatistics Coordinating Center of George Washington University, Washington, DC. Detailed description of methods and subjects’ enrollment has been reported.^12,13 The study had approval from the Institutional Review Board of each participating institution.

Mother–infant dyads from singleton gestations were recruited from May 1993 to May 1995, if infant’s birth weight was at least 500 g and gestational age was less than 43 weeks by best obstetric estimate. Mothers were approached in the hospital after delivery, informed consent obtained, and then they were interviewed briefly for history of smoking, alcohol consumption, and drug use during pregnancy and in the last year. At interview, tobacco use during pregnancy was categorized into no smoking, some smoking (less than half a pack per day), or heavy smoking (at least half a pack per day), and alcohol consumption into no alcohol, some alcohol (less than one drink per month), moderate alcohol (1–3 drinks per month), or heavy alcohol drinking (at least one drink per week). A separate question asked whether more than five drinks were consumed on any given day (binge). Mothers were also asked about their date of first prenatal care visit, number of visits, and prepregnancy weight.

Meconium was collected and the presence of metabolites determined by gas chromatography/mass spectroscopy.¹³ Trained and certified research staff masked to exposure status performed physical examination and obtained growth measurements on the infants. Maternal and infant medical records were abstracted for information on treatment, procedures, diagnoses, maternal age, weight at delivery admission, hospitalization during pregnancy, and reproductive history. We dichotomized prenatal care into inadequate or intermediate and adequate care, based on the Kessner Index.¹⁴ Reproductive history was defined as abnormal if parity was >5 or if a mother had >2 previous premature births or abortions.

We defined cocaine exposure as maternal self-report of cocaine use during pregnancy or meconium analysis yielded cocaine metabolites. Cocaine-negative infants were those born to mothers who denied cocaine use, with confirmation by a negative meconium analysis. Opiate exposure was similarly determined. All statistical analyses were done using SAS statistical software (SAS Institute Inc., Cary, NC). Exploratory statistical analyses compared demographic and other characteristics between cocaine-exposed and cocaine-negative infants using t test (continuous variables) or ² test (categorical factors). A nonparametric method (Kolmogorov–Smirnov) was used to compare equality of distributions between cocaine-exposed and cocaine-negative groups. Percentile estimates for each growth parameter, (birth weight, length, and head circumference) at each gestational age determined by best obstetric estimate were also graphically compared. These explorations indicated that cocaine-associated deviation in growth measurements started to become evident after 32 weeks’ gestation. Thus, subsequent analyses were carried out after stratifying the data into gestational ages 32 weeks and > 32 weeks.

Multivariate regression models were used to obtain adjusted effects of cocaine exposure that controlled for potential confounders. Likely confounders (clinical site, opiate use, smoking, alcohol, and marijuana use) were always adjusted for, regardless of statistical significance. In addition, other variables or potential confounders were adjusted for only if they were statistically significant. These possible confounders included race, gender, gestational age, interaction terms (cocaine x gestational age, opiate x gestational age, cocaine x alcohol, cocaine x opiate), and maternal factors: age, Medicaid insurance, prenatal care, weight gain during pregnancy, preeclampsia, hematologic disorders, abnormal reproductive history, oligo-polyhydramnios, sexually transmitted diseases, acquired immune deficiency, thyroid dysfunction, any hepatitis, diabetes (insulin dependent), seizure disorder, chronic hypertension, and any hospitalization during pregnancy. A backward selection algorithm was used to eliminate those possible confounders that were not statistically significant. For each categorical factor with more than two levels that was significant, pair-wise comparison was carried out to determine the precise nature of the differences between levels of that factor.

	RESULTS

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A total of 19,079 mother–infant dyads were screened for study recruitment. Of these, 16,988 dyads were eligible for enrollment, and 11,811 (70%) mothers gave consent. One thousand seventy-two (1072) infants were cocaine exposed, whereas 7565 were confirmed cocaine negative. The remaining 3174 infants were born to mothers who denied cocaine use, but history was unconfirmed because insufficient or no meconium was collected. This group was excluded from the analysis. Table 1 shows that maternal and infant characteristics of this group were similar to the cocaine-negative group. It also shows that mothers and infants in the cocaine-positive group were significantly different from the cocaine-negative group. Tobacco, alcohol, marijuana, and opiate use were present in both groups, though the respective prevalence was much higher in the cocaine-positive group.

View larger version (30K): [in this window] [in a new window]   Figure 1. A) Birth weight frequency distribution of cocaine-exposed (cocaine+) infants compared to the cocaine-negative (cocaine-) group. B–D) Percentile estimates (10th, 50th, and 90th) for birth weight, birth length, and head circumference, respectively, for each gestational age comparing the cocaine+ and cocaine- groups. Bada. Cocaine and Birth Measurements. Obstet Gynecol 2002.

View this table: [in this window] [in a new window]   Table 2. Results of Multivariate Regression Analyses Showing the Adjusted Effects of Cocaine Exposure on Growth Measurements and Gestational Ages 32 Weeks and 32 Weeks

	DISCUSSION

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In utero exposure to illicit drugs, including cocaine, is reported to be associated with increased incidence of low birth weight (weight < 2500 g),^6,8,11 shortened gestation,^15,16 lower mean birth weight,^3–5 or weight less than the tenth or the 20th percentile of a commonly referenced intrauterine growth curve.^5,6,17 The large number in our study provided us with a rich data set, enabling us to characterize more comprehensively infant growth following gestational cocaine exposure, while controlling for confounders known to negatively impact fetal growth.

In term or near-term infants, cocaine exposure has been reported to result in the shift of birth weight and head circumference to the lower percentile.^5,17 A moderating effect by gestational age on the impact of drug exposure on weight and length but not head circumference was reported by Brown et al,¹⁸ who observed more extreme growth deficits at term gestation. With rapid growth velocity in the fetus after 30 weeks’ gestation,¹⁹ any negative impact of cocaine on growth would likely result in restriction or deceleration that becomes more evident at later weeks of gestation. In fact, as evidenced by the statistically significant interaction terms between cocaine and gestational age, growth restriction became more pronounced as gestation approached term.

We further observed that the negative impact of cocaine on growth remained significant after adjusting for the effects of opiate, tobacco, alcohol, marijuana, and other factors. Zuckerman et al⁴ found that gestational cocaine exposure was associated with a decrease in weight, length, and head circumference, and these measurements negatively correlated with the number of cigarettes smoked per day but not with the daily volume of alcohol intake. Our findings are consistent with their results, but we also found a negative effect of heavy alcohol use at later gestation. Jacobson et al²⁰ observed larger deficits in birth weight related to heavy drinking compared with deficits from heavy smoking and that cocaine effects were attributable to shortened gestation. In our sample, the negative impact of alcohol on growth was of lesser magnitude than the effects of smoking or cocaine, and the effect of cocaine was not attributable to shortened gestation.

Decreased growth measurements in cocaine exposure have been attributed to maternal and obstetric risk factors, sociodemographic factors, lack of prenatal care, and undernutrition.^3,4,11,21 In our study, growth measurements were significantly decreased in blacks, girls, and those with maternal medical or obstetric complications. Our mothers on Medicaid had infants with smaller head size; low socioeconomic status has been correlated with small head size and poor neurological outcome.²² Of interest was our finding of brain sparing with preeclampsia early in gestation, evolving into symmetrical growth restriction at later gestation. In cocaine-exposed infants, the incidence of low birth weight has been reported to decrease with increased number of prenatal care visits.²¹ MacGregor et al¹⁵ found improved growth measurements with comprehensive prenatal care. We also found higher growth measurements with adequate prenatal care in infants born after 32 weeks, but an inverse relationship was noted between prenatal care and growth during gestation 32 weeks. Health behavior may have been a factor (ie, mothers sought early care because of complications, necessitating more visits). Richardson et al²³ found no effect of prenatal care on birth weight following prenatal cocaine exposure; however, the true impact of prenatal care may not be evident, because prenatal care utilization may not indicate content of services received.²⁴

Growth restriction associated with in utero cocaine exposure may be explained by undernutrition.²⁵ We found that maternal weight gain during pregnancy was not significantly related to growth measurements. Our mothers may possibly have had poor recall of their prepregnancy weight, and we were unable to detect the true relationship between maternal weight gain and intrauterine growth. Moreover, factors such as endocrine influences have been suggested in the mechanism of growth deceleration in cocaine exposure.^26–30

In some reports,^9,10 the head size of drug-exposed infants was noted to be disproportionately smaller than expected for body weight and length,³⁰ a reverse pattern of asymmetrical growth restriction.⁹ However, many studies^{5,16,23,31,32} including ours found symmetrical growth restriction following gestational cocaine exposure. Dose–effect relationship has been reported between newborn head circumference and concentrations of cocaine metabolite (benzoylecgonine) in maternal³³ or neonatal hair.³⁴ We used gas chromatography/mass spectroscopy for meconium testing, and qualitative and quantitative differences in metabolites detected were observed in different infants.¹³ Thus, it would have been problematic in our study to look for dose-effects based on meconium results. Because drug metabolites in meconium are likely to represent exposure in the later months of pregnancy, our infants could have been exposed for several months’ duration (ie, throughout gestation or equivalent to heavy exposure). The mean decrease in head size noted in our cocaine-exposed infants at 40 weeks’ gestation is comparable to Bateman and Chiriboga’s³³ observation of -0.44 ± .17-cm decrease in head circumference in babies exposed to high levels of cocaine. Kuhn et al³⁵ found a dose–response relationship between cocaine concentrations in maternal hair and birth weight but not head size. We could have investigated dose of exposure at recruitment through a detailed maternal interview of drug use by month or trimester of pregnancy, but this was precluded by the large number of subjects enrolled in the Maternal Lifestyle Study.

The exclusion of infants with unconfirmed negative exposure status from analysis may be a source of bias; however, these infants were likely nonexposed, because, in addition to a negative maternal self-report, infant and maternal characteristics for this group were similar to the cocaine-negative group. Furthermore, in this population, the probability of cocaine confirmation by meconium testing, given that a mother denied use, is only .024.¹³ Our findings, therefore, likely represent underestimates of the true association between cocaine and growth restriction.

Because of variability in population characteristics and prevalence of cocaine use among clinical centers, we controlled for clinical site in our analysis; however, generalizability of our findings is limited because our study population was drawn from urban areas, with a large proportion of low socioeconomic status. Despite this limitation, our large sample, confirmation of exposure by meconium analysis using a highly specific and sensitive method, rigorous training and masking of research personnel to exposure status, and controlling for multiple confounders, lead us with a high degree of confidence to conclude that in utero cocaine exposure is associated with fetal growth restriction involving all birth measurements.

Unless growth measurements are below the tenth percentile of a reference growth curve,^36–39 the impact of drug use on fetal growth would not be as evident in the newborn period. Exposed infants may have measurements above the tenth percentile and anthropometrically similar to nonexposed infants. Based on the United States national reference for fetal growth,³⁹ 10% of infants are born with birth weight less than 2929 g. A 151-g mean downward shift in birth weight due to cocaine exposure will result in a three-fold increase (to 32%) in the prevalence of infants born with weight less than tenth percentile. Compounding the effects of cocaine are the independent negative impact of frequently co-occurring factors, such as smoking, alcohol, opiates, abnormal reproductive history, and lack of prenatal care.

The long-term impact of cocaine on growth deviation will need to be determined in the context of exposure to both prenatal and postnatal factors.⁴⁰ The follow-up phase of our study has been designed to address some of these concerns. Our findings support the need to achieve many objectives of Healthy People 2010. To address the problem of low birth weight, early access to prenatal care will likely detect medical and obstetric complications and provide intervention toward smoking cessation and alcohol and drug treatment. From the public health perspective, a greater impact on decreasing rates of low birth weight can be achieved by continued and expanded primary prevention programs against tobacco, alcohol, and drug use specifically directed to children and youth.

	Footnotes

 
Supported by National Institutes of Health (NIH) National Institute of Child Health and Human Development through cooperative agreements: U10HD27856 (to HSB), U01HD36790 (to AD), U10HD21397 (to CRB), U10HD21385 (to SS), U10HD27904 (to BL), and U01HD19897 (to JV); and interagency agreement with the National Institute on Drug Abuse (NIDA), Administration for Children, Youth and Families (ACYF), and Center for Substance Abuse Treatment (CAST).

PII S0029-7844(02)02199-3

Received February 28, 2002. Received in revised form May 13, 2002. Accepted June 6, 2002.

	REFERENCES

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
1. Substance Abuse and Mental Health Services Administration, Office of Applied Studies. Summary of findings from the 2000 National Household Survey on Drug Abuse. Washington, DC: Department of Health and Human Services, 2001.

2. Births, marriages, divorces, and deaths: Provisional data for January–December 2000. Natl Vital Stat Rep 2001;49: 1–8.[Medline]

3. Coles CD, Platzman KA, Smith I, James ME, Falek A. Effects of cocaine and alcohol use in pregnancy on neonatal growth and neurobehavioral status. Neurotoxicol Teratol 1992;14:23–33.[Medline]

4. Zuckerman B, Frank DA, Hingson R, Amaro H, Levenson SM, Kayne H, et al. Effects of maternal marijuana and cocaine use on fetal growth. N Engl J Med 1989;320: 762–8.[Abstract]

5. Hadeed AJ, Siegel SR. Maternal cocaine use during pregnancy: Effect on the newborn infant. Pediatrics 1989;84: 205–10.[Abstract/Free Full Text]

6. Chouteau M, Namerow PB, Leppert P. The effect of cocaine abuse on birth weight and gestational age. Obstet Gynecol 1988;72:351–4.[Abstract/Free Full Text]

7. Eyler FD, Behnke M, Conlon M, Woods NS, Wobie K. Birth outcome from a prospective, matched study of prenatal crack/cocaine use: I. Interactive and dose effects on health and growth. Pediatrics 1998;101:229–37.[Abstract/Free Full Text]

8. Eyler FD, Behnke M, Conlon M, Woods NS, Frentzen B. Prenatal cocaine use: A comparison of neonates matched on maternal risk factors. Neurotoxicol Teratol 1994;16: 81–7.[Medline]

9. Little BB, Snell LM. Brain growth among fetuses exposed to cocaine in utero: Asymmetrical growth retardation. Obstet Gynecol 1991;77:361–4.[Abstract/Free Full Text]

10. Scafidi FA, Field TM, Wheeden A, Schanberg S, Kuhn C, Symanski R, et al. Cocaine-exposed preterm neonates show behavioral and hormonal differences. Pediatrics 1996;97:851–5.[Abstract/Free Full Text]

11. Kistin N, Handler A, Davis F, Ferre C. Cocaine and cigarettes: A comparison of risks. Pediatr Perinatal Epidemiol 1996;10:269–78.[Medline]

12. Bauer CR, Shankaran S, Bada HS, Lester B, Wright LL, Krause-Steinrauf H, et al. Maternal Lifestyle Study: Drug exposure during pregnancy and short-term maternal outcomes. Am J Obstet Gynecol 2002;186:487–95.[Medline]

13. Lester BM, ElSohly M, Wright LL, Smeriglio VL, Verter J, Bauer CR, et al. The Maternal Lifestyle Study: Drug use by meconium toxicology and maternal self-report. Pediatrics 2001;107:309–17.[Abstract/Free Full Text]

14. Kessner D. Infant death: An analysis by maternal risk and health care. Institute of Medicine, Contrasts in Health Status. Volume I. Washington, DC: National Academy of Sciences, 1973:58–60.

15. MacGregor SN, Keith LG, Bachicha JA, Chasnoff IJ. Cocaine abuse during pregnancy: Correlation between prenatal care and perinatal outcome. Obstet Gynecol 1989;74:882–4.[Abstract/Free Full Text]

16. Oro AS, Dixon SD. Perinatal cocaine and methamphetamine exposure: Maternal and neonatal correlates. J Pediatr 1987;111:571–8.[Medline]

17. Hurt H, Brodsky NL, Braitman LE, Giannetta J. Natal status of infants of cocaine users and control subjects: A prospective comparison. J Perinatol 1995;15:297–304.[Medline]

18. Brown JV, Bakeman R, Coles CD, Sexson WR, Demi AS. Maternal drug use during pregnancy: Are preterm and full-term infants affected differently? Dev Psychol 1998; 14:540–54.

19. Sparks JW, Girard JR, Battaglia FC. An estimate of the caloric requirements of the human fetus. Biol Neonate 1980;38:113–9.[Medline]

20. Jacobson JL, Jacobson SW, Sokol RJ, Martier SS, Ager JW, Shankaran S. Effects of alcohol use, smoking, and illicit drug use on fetal growth in black infants. J Pediatr 1994; 124:757–64.[Medline]

21. Racine A, Joyce T, Anderson R. The association between prenatal care and birth weight among women exposed to cocaine in New York City. JAMA 1993;270:1581– 6.[Abstract]

22. Gross SJ, Kosmetatos N, Grimes CT, Williams ML. Newborn head size and neurological status. Am J Dis Child 1978;132:753–6.[Abstract]

23. Richardson GA, Hamel SC, Goldschmidt L, Day NL. Growth of infants prenatally exposed to cocaine/crack: Comparison of a prenatal care and a no prenatal care sample. Pediatrics 1999;104:1–10.[Abstract/Free Full Text]

24. Kotelchuck M. An evaluation of the Kessner adequacy of prenatal care index and a proposed adequacy of prenatal care utilization index. Am J Public Health 1994;84: 1414–20.[Abstract/Free Full Text]

25. Knight EM, Hutchinson J, Edwards CH, Spurlock BG, Oyemade UJ, Johnson AA, et al. Relationships of serum illicit drug concentrations during pregnancy to maternal nutritional status. J Nutr 1994;124:973S–80S.

26. Church MW, Jen K-L, Pellizzon MA, Holmes PA. Prenatal cocaine, alcohol, and undernutrition differentially alter mineral and protein content in fetal rats. Pharmacol Biochem Behav 1998;59:577–84.[Medline]

27. Middaugh LD, Boggan WO, Bingel SA, Patrick KS, Xu W. A murine model of prenatal cocaine exposure: Effects on the mother and the fetus. Pharmacol Biochem Behav 1996;55:565–74.[Medline]

28. Nieto-Diaz A, Villar J, Matorras-Weining R, Valenzuela-Ruiz P. Intrauterine growth retardation at term: Association between anthropometric and endocrine parameters. Acta Obstet Gynecol Scand 1996;75:127–31.[Medline]

29. Price WA, Stiles AD, Moats-Staats BM, D’Ercole AJ. Gene expression of insulin-like growth factors (IGFs), the type I IGF receptor, and IGF-binding proteins in dexamethasone-induced fetal growth retardation. Endocrinology 1992;130:1424–32.[Abstract]

30. McGivern RF, Fatayerji N, Handa RJ. Androstenedione synergizes with stress or prenatal drug exposure to retard fetal growth: Role of IGF. Pharmacol Biochem Behav 1996;55:549–57.[Medline]

31. Frank DA, Bauchner H, Parker S, Huber AM, Kyei-Aboagye K, Cabral H, et al. Neonatal body proportionality and body composition after in utero exposure to cocaine and marijuana. J Pediatr 1990;117:622–6.[Medline]

32. Bandstra ES, Morrow CE, Anthony JC, Churchill SS, Chitwood DC, Steele BW, et al. Intrauterine growth of full-term infants: Impact of prenatal cocaine exposure. Pediatrics 2001;108:1309–19.[Abstract/Free Full Text]

33. Bateman DA, Chiriboga CA. Dose-response effect of cocaine on newborn head circumference. Pediatrics 2000; 106:1–6.[Abstract/Free Full Text]

34. Sallee FR, Katikaneni LP, McArthur PD, Ibrahim HM, Nesbitt L, Sethuraman G. Head growth in cocaine-exposed infants: Relationship to neonate hair level. J Dev Behav Pediatr 1995;16:77–81.[Medline]

35. Kuhn L, Ng S, Levin B, Susser M. Cocaine use during pregnancy and intrauterine growth retardation: New insights based on maternal hair tests. Am J Epidemiol 2000;152:112–9.[Abstract/Free Full Text]

36. Lubchenco LO, Hansman C, Boyd E. Intrauterine growth in length and head circumference as estimated from live births at gestational ages from 26 to 42 weeks. Pediatrics 1966;37:403–8.[Abstract/Free Full Text]

37. Usher R, McLean F. Intrauterine growth of live-born Caucasian infants at sea level: Standards obtained from measurements in 7 dimensions of infants born between 25 and 44 weeks of gestation. J Pediatr 1969;74:901–10.[Medline]

38. Babson SG, Benda GI. Growth graphs for the clinical assessment of infants of varying gestational age. J Pediatr 1976;89:814–20.[Medline]

39. Alexander GR, Himes JH, Kaufman RB, Mor J, Kogan M. A United States national reference for fetal growth. Obstet Gynecol 1996;87:163–8.[Abstract]

40. Frank DA, Augustyn M, Knight WG, Pell T, Zuckerman B. Growth, development, and behavior in early childhood following prenatal cocaine exposure. JAMA 2001; 285: 1613–25.[Abstract/Free Full Text]

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