Severity of prenatal cocaine exposure and child language functioning through age seven years: a longitudinal latent growth curve analysis

The current study estimates the longitudinal effects of severity of prenatal cocaine exposure on language functioning in an urban sample of full-term African-American children (200 cocaine-exposed, 176 noncocaine-exposed) through age 7 years. The Miami Prenatal Cocaine Study sample was enrolled prospectively at birth, with documentation of prenatal drug exposure status through maternal interview and toxicology assays of maternal and infant urine and infant meconium. Language functioning was measured at ages 3 and 5 years using the Clinical Evaluation of Language Fundamentals--Preschool (CELF-P) and at age 7 years using the Core Language Domain of the NEPSY: A Developmental Neuropsychological Assessment. Longitudinal latent growth curve analyses were used to examine two components of language functioning, a more stable aptitude for language performance and a time-varying trajectory of language development, across the three time points and their relationship to varying levels of prenatal cocaine exposure. Severity of prenatal cocaine exposure was characterized using a latent construct combining maternal self-report of cocaine use during pregnancy by trimesters and maternal and infant bioassays, allowing all available information to be taken into account. The association between severity of exposure and language functioning was examined within a model including factors for fetal growth, gestational age, and IQ as intercorrelated response variables and child's age, gender, and prenatal alcohol, tobacco, and marijuana exposure as covariates. Results indicated that greater severity of prenatal cocaine exposure was associated with greater deficits within the more stable aptitude for language performance (D = -0.071, 95% CI = -0.133, -0.009; p = 0.026). There was no relationship between severity of prenatal cocaine exposure and the time-varying trajectory of language development. The observed cocaine-associated deficit was independent of multiple alternative suspected sources of variation in language performance, including other potential responses to prenatal cocaine exposure, such as child's intellectual functioning, and other birth and postnatal influences, including language stimulation in the home environment.     

Level of prenatal cocaine exposure and infant-caregiver attachment behavior

The objective of this longitudinal prospective cohort study was to determine whether level of prenatal cocaine exposure, or the interaction between level of prenatal cocaine exposure and contextual risk variables, was associated with a higher rate of infant-caregiver insecure attachment and disorganized attachment, or with alterations in infant crying or avoidant behavior, after controlling for prenatal exposure to alcohol, tobacco, and marijuana, the quality of the proximal caregiving environment, and other covariates. Subjects were 154 full-term 12-month-old infants (64 unexposed, 61 with lighter cocaine exposure, 29 with heavier cocaine exposure) and their primary caregivers from low-income, urban backgrounds. Exposure status was determined in the maternity ward by biologic assay (infant meconium and/or maternal or infant urine) and maternal self-report. At the 12-month follow-up visit, infants were videotaped with their primary caregiver in Ainsworth's Strange Situation. Reliable coders masked to exposure status scored videotapes for attachment variables, amount of crying, and level of avoidance. Contrary to popular perceptions, level of prenatal cocaine exposure was not significantly related to secure/insecure attachment status, disorganized attachment status, or rated level of felt security. Foster care status also was not associated with attachment status. However, heavier prenatal cocaine exposure, in interaction with maternal contextual variables (public assistance or multiparity) was associated with alterations in infant socio-affective behavior, including a higher level of behavioral disorganization, more avoidance of the caregiver, and less crying.     

Prenatal cocaine exposures and dose-related cocaine effects on infant tone and behavior

BACKGROUND: In experimental models, prenatal cocaine exposure has been found to perturb monoaminergic development. In humans, numerous studies have sought clinical correlates, but few have focused on dose-related effects, especially as regards neurologic function beyond the neonatal period. OBJECTIVE: To assess whether prenatal cocaine exposure has adverse effects on infant neurologic, developmental and behavioral outcomes and whether any effects are dose-dependent. DESIGN/METHODS: Infants (398) were enrolled at birth from an urban hospital. Drug exposure was ascertained with biomarkers in hair (n=395), urine (n=170) and meconium (n=109). Children were followed prospectively and 286 (72%) were evaluated blind to drug exposure at 6 months of age with the Bayley scales, Fagan Scale of Infant Intelligence and a standardized neurological examination. RESULTS: Certain neurological findings increased significantly by the amount of cocaine detected in maternal hair, e.g. abnormality of tone, as indicated by extensor posture was detected among 28% of cocaine-unexposed infants, 43% of infants exposed to lower and 48% exposed to higher cocaine levels in maternal hair (p<0.009). Persistent fisting increased in a similar dose-dependent manner. These associations persisted in adjusted analyses. Prenatal cocaine exposure was not associated with developmental scores (mental, motor or novelty preference) but was associated with lower orientation scores in adjusted analyses. CONCLUSIONS: At 6 months of age, prenatal cocaine exposure was associated with abnormalities of tone and posture and with lower orientation scores. Perturbations in monoaminergic systems by cocaine exposure during fetal development may explain the observed neurological and behavioral symptoms. Whether such findings in infancy increase the risk of later neurobehavioral problems requires further study.     

Effects of cocaine and alcohol use in pregnancy on neonatal growth and neurobehavioral status.

Effects on fetal growth and neonatal behavior of cocaine and alcohol use in pregnancy were investigated in infants born to women in a low-income, predominantly black population. Despite the increased use of cocaine by pregnant women and the accompanying public concern, behavioral studies of exposed neonates are limited in number and scope. In most studies, confounding factors (e.g., polydrug abuse, prematurity, infant health status) have not been controlled so the actual effects of cocaine and other drug exposure are not clear. Accordingly, this study investigated effects of prenatal drug exposure although controlling experimentally for other factors known to be associated with poor outcomes in infants: prematurity, other illicit drug use, associated diseases (e.g., sexually transmitted diseases [STDs]), and duration of drug use. In addition, other factors statistically controlled were: experimenter effects, timing of assessment, and effects of duration, amount, and frequency of cocaine, alcohol, marijuana, and nicotine exposure. One hundred and seven full-term infants were assessed at 2, 14, and 28 days using the Brazelton Neonatal Behavioral Assessment Scale (BNBAS) by testers blind to infant status. Growth factors (i.e., birthweight, length, head circumference) were also assessed.     

Longitudinal influence of prenatal cocaine exposure on child language functioning

The present study estimates the longitudinal effects of in utero cocaine exposure on language functioning at 3, 5 and 7 years of age in an urban sample of 443 full-term children (236 cocaine-exposed and 207 noncocaine-exposed) participating in the Miami Prenatal Cocaine Study. The sample was enrolled prospectively at birth, with documentation of prenatal drug exposure status through maternal interview and urine and meconium toxicology assays. Language functioning was measured at ages 3 and 5 years using the Clinical Evaluation of Language Fundamentals-Preschool (CELF-P) and at age 7 years using the Core Language Domain of the NEPSY: A Developmental Neuropsychological Assessment. Longitudinal Generalized Linear Model and Generalized Estimating Equations (GLM/GEE) analyses revealed an association between prenatal cocaine exposure and deficits in total language functioning after statistically controlling for child sex, visit age, prenatal exposure to alcohol, marijuana and tobacco and over 20 additional medical and sociodemographic covariates drawn from potentially confounding influences assessed at birth and follow-up visits (D=-0.17; 95% CI=-0.32, -0.03; P=.019). The link from prenatal cocaine exposure to later language deficits does not appear to be mediated by cocaine-associated deficits in birth weight, length or head circumference. Overall, the evidence tends to support an inference of a stable cocaine-specific effect on indicators of language functioning during early childhood through age 7 years.     

Estimated effects of in utero cocaine exposure on language development through early adolescence

The potential longitudinal effects of prenatal cocaine exposure (PCE) on language functioning were estimated from early childhood through early adolescence in a large, well-retained urban sample of 451 full-term children (242 cocaine-exposed, 209 non-cocaine-exposed) participating in the Miami Prenatal Cocaine Study (MPCS). The sample was enrolled prospectively at birth, with documentation of prenatal drug exposure status through maternal interview, and toxicology assays of maternal and infant urine, and infant meconium. Age-appropriate versions of the Clinical Evaluation of Language Fundamentals (CELF) were used to measure total, expressive, and receptive language at ages 3, 5, and 12 years. Longitudinal latent growth curve (LLGC) modeling of the data revealed an association between PCE (measured dichotomously as yes/no) and lower functioning in expressive and total language scores, after considering other sources of variation including child's age at testing, sex, prenatal exposure to alcohol, marijuana, and tobacco, and additional medical and social-demographic covariates. Analyses of level of PCE showed a gradient, i.e. dose-dependent, relationship between PCE level and expressive, receptive, and total language scores in the models controlling for age, child's sex, and other prenatal drug exposures. With additional covariate control these findings were most stable for the total language score. The evidence supports an inference about an enduring stable cocaine-specific effect on children's language abilities, with no effect on language growth over time in the longitudinal trajectory of language development.     

Longitudinal investigation of task persistence and sustained attention in children with prenatal cocaine exposure

The present study estimates the longitudinal effects of prenatal cocaine exposure on indicators of sustained attention processing at 3, 5 and 7 years of age in an urban sample of full-term African–American children (235 cocaine-exposed, 207 noncocaine-exposed). The sample was enrolled prospectively at birth, with documentation of prenatal drug exposure status through maternal interview, urine and meconium toxicology assays. Sustained attention was measured at age 3 years using a standardized measure of task persistence during a challenging task [G.A. Morgan, N.A. Busch-Rossnagel, C.A. Maslin-Cole and R.J. Harmon, Individualized Assessment of Mastery Motivation: Manual for 15–36 Month Old Children, 1992.], and at ages 5 and 7 years using omission error scores from computerized continuous performance tasks (CPT) [L. Greenberg, R. Leark, T. Dupuy, C. Corman, C. Kindschi, M. Cenedela, Test of Variables of Attention (T.O.V.A. and T.O.V.A.-A.), 22, Universal Attention Disorders, Los Alamitos, CA, 1996; C.K. Conners, Conners' Continuous Performance Test (CPT), second ed., Multi-Health Systems, Canada, 1995.]. Findings from longitudinal GLM/GEE analyses of the three measured time points support a stable influence of prenatal cocaine exposure on indicators of sustained attention, after controlling for prenatal exposure to alcohol, marijuana, tobacco and over 20 additional medical and social–demographic covariates drawn from potentially confounding influences assessed at birth and later assessment visits (D=0.21; 95% CI=0.04, 0.38; P=.017). This effect was not mediated by fetal growth or gestational age and remained highly stable with increasing levels of covariate control. Separately, using the age 7 data, a structural equations model (SEM) was constructed combining all available self-report and bioassay data to measure magnitude of cocaine exposure in relationship to attention task performance. Results indicated a gradient of influence, with each standard deviation increase in the level of prenatal cocaine exposure relating to a 16% standard deviation increase in omission error scores at age 7. Overall findings support a stable cocaine-specific effect on indicators of sustained attention processing during the early childhood years. Results are discussed within the context of neurobiological and behavioral research linking prenatal cocaine exposure to long-lasting disruption of the brain systems subserving arousal and attention.     

Maternal cocaine use and mother-infant interactions: Direct and moderated associations

This study examined the associations between prenatal cocaine exposure and quality of mother-infant play interactions at 13 months of infant ages. We investigated whether maternal psychological distress and infant reactivity mediated or moderated this association. Participants consisted of 220 (119 cocaine exposed and 101 non-cocaine exposed) mother-infant dyads participating in an ongoing longitudinal study of prenatal cocaine exposure. Results indicated that mothers who used cocaine during pregnancy displayed higher negative affect and lower sensitivity toward their infant during play interactions at 13 months, and that their infants were less responsive toward them. Contrary to hypothesis, this association was not mediated by maternal psychological distress or by infant reactivity. However, results for both the cocaine and non-cocaine exposed infants were supportive of a transactional model where lower maternal sensitivity at 1 month was predictive of higher infant reactivity at 7 months, which in turn was predictive of lower maternal warmth/sensitivity at 13 months, controlling for potential stability in maternal behavior. Results also indicated that as hypothesized, infant reactivity moderated the association between maternal cocaine use during pregnancy and maternal warmth/sensitivity at 13 months of age. Cocaine-using mothers who experienced their infants as being more reactive in early infancy were less warm/sensitive toward them in later infancy. Results have implications for parenting interventions that may be targeted toward improving maternal sensitivity among cocaine-using mothers with more reactive infants.     

Newborn evaluations of toxicity and withdrawal related to prenatal cocaine exposure.

The literature on prenatal cocaine exposure is unclear whether immediate postpartum effects on the infant are transient, related to either acute toxicity of cocaine, or to a withdrawal effect as cocaine is metabolized, or whether they might persist. This prospective, longitudinal study was designed to test the hypotheses that newborns urine-positive for cocaine metabolites, compared to those exposed but urine-negative, and to nonexposed controls would (1) have poorer neurobehavioral scores (toxicity effect) and (2) worsen or demonstrate less improvement over the first week (withdrawal effect). We approached over 2500 pregnant women designated to deliver at our referral hospital from public health clinics; 85% consented to participate in a longitudinal study. We excluded women <18 years old with major chronic illness and prenatal drug use except cocaine, marijuana, alcohol and tobacco. From positive urine toxicologies or admissions in private, thorough interviews, 154 were identified as prenatal cocaine users; 154 were selected from noncocaine users matched on socioeconomic status (SES), race, parity and location of prenatal care (that related to perinatal risk), for a total sample size of 308. Included in this article are the 155 surviving infants who were full-term, delivered vaginally and were well and available for testing over the first week postpartum. Infant urine specimens were collected, and neurobehavorial testing was performed by certified, blinded examiners using the Neonatal Behavioral Assessment Scale on days 1, 2-4 and 5-7 postpartum. In toxicity analyses, controlling for amount of prenatal drug exposures, only autonomic regulation demonstrated significant overall and cocaine drug group effects. Urine-positive newborns had the poorest scores (i.e., more startles, tremors). However, given that planned comparisons were not significant, these data provided little support for acute toxicity effects. In withdrawal analyses, only one significant change over time varied among exposure groups. Those infants exposed and positive for cocaine metabolites increased their scores on regulation of state on days 2-4 and decreased them on days 5-7 (when withdrawal might be evident). However, their scores on days 5-7 were not significantly lower than their initial scores, nor different from the days 5-7 scores of the exposed negatives or control infants, lending little support for withdrawal effects. Our data support those of other controlled studies in failing to demonstrate devastating early effects of prenatal cocaine exposure. They add to our understanding that effects observed do not appear to be related to acute toxicity nor to cocaine withdrawal. The uncertainty of persistent effects of cocaine exposure warrants long-term follow-up.     

Oxidative stress in pregnant women and birth weight reduction

The purpose of this study is to evaluate the role of maternal oxidative stress in lowering neonatal birth weight. Women (N = 261) with singleton pregnancy were analyzed for biomarker levels of oxidative stress after recruitment at the time of hospitalization for delivery in Korea between 2000 and 2001. Among the neonates, 247 births were full-term infants and 14 births were pre-term infants. Biomarkers measured for oxidative stress were maternal urinary 8-hydroxydeoxyguanosine (8-OH-dG) and malondialdehyde (MDA). The women with pre-term infants had higher concentrations of urinary 8-OH-dG and MDA than those with full-term babies. The concentrations of maternal urinary 8-OH-dG and MDA were inversely associated with birth weight of full-term deliveries after adjusting for potential confounders including maternal age, body mass index, dietary intake, alcohol consumption, smoking exposure, occupational status, and neonatal sex (P < 0.05). This study demonstrates that increase of 8-OH-dG and MDA concentrations in urine of pregnant women were associated with reduced birth weight in full-term deliveries.     

Relative ability of biologic specimens and interviews to detect prenatal cocaine use

For this study, we recruited women admitted to our labor and delivery service, enrolling all consenting patients with a history of prenatal cocaine use and the next admission with no recorded use. During the immediate postpartum period, experienced researchers conducted private, structured interviews to obtain details of prenatal cocaine use and to identify a priori exclusion criteria (other illicit drug use, high alcohol use and chronic illnesses and medications). Specific protocols were used to collect amniotic fluid, cord blood, infant urine, meconium and maternal hair. All specimens were analyzed blind with respect to exposure using gas chromatography/mass spectrometry. Of 115 subjects, 46 had one or more biologic specimens positive for cocaine metabolites and five admitted prenatal use, but had negative specimens. Of these 51 identified as users by any method, 38 admitted, 32 were positive for urine, 28 for hair and 25 for meconium. Of the 38 admitters, 87% had positive specimens; of the 77 denying use, 17% were positive. Urine was most frequently positive in identified users, 67% overall and 62% of users who denied. Hair was next, positive in 65% of all users and 50% of users who denied. Of the 13 subjects who denied use but were positive on at least one specimen, four were identified solely by urine, two only by hair and one only by meconium. Self-report identified five users with all negative specimens. Although no one method identified all users, the single method that maximally identified users was detailed history taken by experienced interviewers.     

Effects of cocaine/polydrug exposure and maternal psychological distress on infant birth outcomes

To assess teratogenic effects of cocaine exposure and maternal psychological distress on birth outcomes, we conducted a longitudinal prospective study of 415 infants (218 cocaine-exposed--CE, 197 nonexposed--NE). Drug exposure was determined through a combination of maternal self-report, urine, and meconium screens. Maternal psychological distress postpartum was evaluated through a standardized, normative, self-report assessment. An extensive set of confounding variables was controlled, including severity of exposure to alcohol, tobacco, marijuana and other drugs, maternal age, race, parity, number of prenatal care visits, educational, marital, and socioeconomic status, and verbal and nonverbal intelligence. CE infants were smaller on all birth parameters and more likely to be preterm, small for gestational age, and microcephalic than NE infants. Forty-one percent of cocaine users had clinically significant psychological symptoms, compared to 20% of a high-risk comparison group of noncocaine users. Consistent with a teratologic model, cocaine exposure independently predicted offspring birthweight, length, and head circumference. Maternal psychological distress self-reported postnatally also independently predicted head circumference. Tobacco, alcohol, and marijuana exposures were also significant independent predictors of some fetal growth parameters. In addition, maternal distress symptoms, which may be reflective of maternal mental health disorders or responses to stress, added significantly to the risk for poorer fetal growth.     

Bioanalysis for cocaine,opiates, methadone,and amphetamines exposure detection during pregnancy

Drug exposure during pregnancy constitutes a major legal issue and a public health concern. Drug and metabolite determination in biological matrices from mother and newborn is an objective indication of prenatal drug exposure. However, limited data are available regarding the interpretation of these analytical results in terms of window of detection and degree of exposure. We collected paired maternal hair, meconium, placenta, and umbilical cord from 727 mother‐newborn dyads. We analyzed these specimens by liquid chromatography‐tandem mass spectrometry for the determination of cocaine, opioids, methadone, and amphetamines, and compared the analytical results from the four different matrices. The cases were divided in non‐exposure, low, and frequent exposure, based on maternal hair concentrations and segmental analysis by trimesters. For cocaine, 62 cases tested positive in hair, 9 in meconium, 6 in placenta and 7 in umbilical cord. In the case of opioids, 14 maternal hair cases were positive, 11 meconium and umbilical cord and 9 placenta samples. For methadone, 11 cases were positive in hair, 9 in meconium and 6 in placenta and umbilical cord. For amphetamines, 18 cases were positive according to maternal hair, but all meconium, placenta, and umbilical cord tested negative. Maternal hair was the most sensitive specimen to detect drug exposure during pregnancy. Meconium, placenta, and umbilical cord tested positive if hair concentrations showed frequent drug use during the whole pregnancy, especially during the third trimester. Meconium, placenta, and umbilical cord also tested positive for morphine and metabolites, if this drug was administered during labour and delivery. Copyright © 2016 John Wiley & Sons, Ltd.     

Maternal and neonatal characteristics following exposure to cocaine in Toronto

We prospectively ascertained gestational cocaine use by neonatal urine and hair tests in 600 mother infant pairs in 3 nurseries in Toronto. The 37 (6.25%) babies who tested positive for cocaine and their mothers were compared to the 563 nonexposed with regard to pregnancy outcome and neonatal complications. Mothers using cocaine were not different in their ages, racial distribution, and obstetric history from those nonexposed. Cocaine-using women had significantly higher risk for vaginal bleeding (16% vs 6%, P < 0.05), hepatitis B carrier state (8% vs 0.8%, P < 0.005), and perhaps more urinary tract infections (8% vs 2.5%, P = 0.08). cocaine-using mothers were significantly more likely to smoke cigarettes (29% vs 10%, P < 0.001). Infants exposed to cocaine in utero were of lower birth weight (3162 ± 645 [SD] g vs 3391 ± 573, P < 0.05) and birth length (49.9 ± 2.9 cm vs 51.1 ± 3.1 cm, P < 0.05). Further stratification of babies exposed to cocaine by maternal cigarette smoking suggests that cigarette smoking accounted for most of this variability [birth weight of babies exposed to cocaine and cigarettes 2899 ± 7.50 g (and 50% of them weighed less than 2500 g), vs 3423 ± 612 (and only 8% less than 2500 g) in those exposed to cocaine only (P < 0.05). Babies exposed to cocaine in utero were significantly more likely to need initial medical support or resuscitation (52% vs 30%, P < 0.05). We conclude that gestational exposure to cocaine, ascertained by a sensitive biologic marker, is associated with substantial perinatal risks. It is probable that some of these risks are caused by clustering of other risk factors such as maternal smoking and hepatitis carrier state. Because routine clinical markers and urine testing often fail to distinguish fetal exposure to cocaine, more common use of the hair test should be considered, especially for babies with complicated perinatal courses.     

Maternal cocaine use and infant behavior

We hypothesized that prenatal cocaine exposure results in less optimal infant behavior and more impaired maternal-infant interaction in healthy term infants. Infants were evaluated with the Neonatal Behavioral Assessment Scale (NBAS) at days 1-3 and 11-30 of age, and mother-infant pairs with the Nursing Child Assessment of Feeding Scale (NCAFS) at 7-16 weeks of age. Drug use was determined from confidential interviews, urine assays and medical records. Cocaine-exposed infants (N = 51) were no different than unexposed comparison infants (N = 60) on the first NBAS exam. On the second NBAS exam, 20 cocaine-exposed infants had slightly lower motor cluster scores compared with those of 32 unexposed infants (p = 0.01), but this difference was reduced after control for several confounding variables. The NCAFS detected no differences between groups in maternal or infant behavior. Infants in this population showed no clinically meaningful effects of cocaine exposure on behavior or maternal-infant interaction.     

Prenatal cocaine use and maternal depression: effects on infant neurobehavior

OBJECTIVE: The present study examined the impact of both perinatal maternal depression and cocaine use on infant neurobehavior at 1 month of age in a large, multi-site study. METHODS: Infant neurobehavior was examined in 1053 infants at 1 month of age using the NICU Network Neurobehavioral Scale (NNNS). Mothers were interviewed using The Addiction Severity Index to determine present and past psychiatric history. Four groups were derived from the total sample: 385 prenatally cocaine-exposed infants, 76 whose mothers reported current postpartum depression (DEP/COC) and 309 without current postpartum depression (nonDEP/COC); 668 infants were not exposed to cocaine, 104 whose mothers reported current postpartum depression (DEP/nonCOC), 564 without current postpartum depression (nonDEP/nonCOC). A 2x2 Analysis of Covariance was used with covariates (birthweight, maternal age, SES, nicotine, alcohol, and research site) to examine infant neurobehavior in these four conditions. Secondary analyses were conducted to examine the effects of amount and timing of prenatal cocaine exposure. RESULTS: DEP group by COC exposure status interactions were significant; there was only a DEP effect in the nonCOC infants. Infants in the nonCOC/DEP group had poorer self-regulation and more stress signs, excitability, and arousal than infants in the other groups. CONCLUSIONS: Postpartum maternal depression has negative effects on infant neurobehavior at 1 month of age. Prenatal cocaine exposure may serve to suppress or buffer the effects of postpartum depression on infant neurobehavior. Maternal mood could explain some of the inconsistencies found in the prenatal cocaine exposure literature.     

Neonatal withdrawal syndrome after chronic maternal drinking of mate

The premature newborn of a mother who reported drinking mate during pregnancy presented with increased jitteriness and irritability, high-pitched cry, hypertonia in the limbs, and brisk tendon reflexes consistent with neonatal withdrawal syndrome. High concentrations of caffeine and theobromine were detected in various maternal and neonatal biological matrices (placenta, cord serum, neonatal urine, maternal and neonatal hair, meconium, and breast milk), demonstrating both acute and chronic prenatal and postnatal exposure to these methylxanthines, contained in high amounts in homemade mate. Symptoms progressively disappeared at 84 hours of age, although intermittent irritability was still present when the infant was discharged at 24 days of age. Fluctuating caffeine (and theobromine) content in different breast milk feeds likely generated the baby's irritability, due to either the physiological stimulatory effects of the methylxanthines or postnatal withdrawal syndrome as the substances cleared from the body. The mother was strongly advised to initiate a considerable, progressive, constant reduction of mate consumption to a maximum of 2 cups a day for the duration of breastfeeding.     

Maternal cocaine use and mother-toddler aggression

This study examined the direct and indirect associations between maternal cocaine use during pregnancy and mother-toddler aggression in an interactive context at 2 years of child age. We hypothesized that in addition to direct effects of cocaine exposure on maternal and child aggression, the association between maternal cocaine use and mother-toddler aggression may be indirect via higher maternal psychiatric symptoms, negative affect, or poor infant autonomic regulation at 13 months. Participants consisted of 220 (119 cocaine exposed, 101 non-cocaine exposed) mother-toddler dyads participating in an ongoing longitudinal study of prenatal cocaine exposure. Results indicated that mothers who used cocaine during pregnancy displayed higher levels of aggression toward their toddlers compared to mothers in the control group. Results from model testing indicated significant indirect associations between maternal cocaine use and maternal aggression via higher maternal negative affect as well as lower infant autonomic regulation at 13 months. Although there were no direct associations between cocaine exposure and toddler aggression, there was a significant indirect effect via lower infant autonomic regulation at 13 months. Results highlight the importance of including maternal aggression in predictive models of prenatal cocaine exposure examining child aggression. Results also emphasize the important role of infant regulation as a mechanism partially explaining associations between cocaine exposure and mother-toddler aggression.     

m-hydroxy benzoylecgonine recovery in fetal guinea pigs.

Recently, meta-hydroxybenzoylecgonine (m-OH BE) was identified by gas chromatography-mass spectroscopy during quantitative analysis for cocaine. Identification of m-OH BE in addition to the routinely identified benzoylecgonine by gas chromatography-mass spectroscopy confirmatory assays may increase detection of cocaine-exposed infants and decrease false negative results. However, it is not known whether m-OH BE is derived directly from benzoylecgonine or from hydroxylated cocaine, or whether this metabolite is produced in the fetus or transferred across the placenta from the maternal circulation. We quantitated the recovery of cocaine, benzoylecgonine, and m-OH BE from amniotic fluid, fetal meconium, fetal intestine, and maternal urine for up to 4 days after single dose administration of either cocaine or benzoylecgonine to pregnant time-bred guinea pigs. m-OH BE was recovered from meconium after maternal injections of cocaine and benzoylecgonine. There was no significant detection of m-OH BE from amniotic fluid or intestine and minimal recovery from maternal urine after either cocaine or benzoylecgonine administration. Detection of m-OH BE in meconium increased the identification of in utero exposed guinea pigs, and the greatest yield of m-OH BE from meconium occurred later than that observed for cocaine or benzoylecgonine.     

Physiological regulation in cigarette exposed infants: an examination of potential moderators

The primary purpose of this study was to examine pathways from prenatal cigarette exposure to physiological regulation at 2 months of age. Specifically, we explored the possibility that any association between prenatal cigarette exposure and infant physiological regulation was moderated by fetal growth, prenatal or postnatal environmental tobacco smoke (ETS) exposure or maternal depressive symptomatology during pregnancy. We evaluated whether exposed infants who were also exposed to ETS after birth, were small for gestational age (SGA) or had mothers with higher depressive symptoms during pregnancy had the highest levels of physiological dysregulation. Respiratory sinus arrhythmia (RSA) was obtained from 234 (166 exposed and 68 nonexposed) infants during sleep. As expected, cigarette-exposed infants had significantly lower RSA than nonexposed infants. This association was not moderated by prenatal or postnatal ETS exposure, or maternal depressive symptomatology during pregnancy. However, small for gestational age status did moderate this association such that nonexposed infants who were not small for gestational age had a significantly higher RSA than nonexposed small for gestational age infants and exposed infants. These findings provide additional evidence that prenatal cigarette exposure is directly associated with dysregulation during infancy.