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Early life stress and environmental influences on the neurodevelopment of children with prenatal opioid exposure.

ABSTRACT: Prenatal opioid exposure has reached epidemic proportions. In the last 10 years, there has been a 242% increase in the number of babies born with the drug withdrawal syndrome known as Neonatal Opioid Withdrawal Syndrome (NOWS). Developmental outcome studies of infants with prenatal opioid exposure are limited by methodological issues including small sample sizes and lack of control for confounding variables such as exposure to poverty and maternal psychopathology. Thus, there is a critical gap in the literature that limits our ability to predict short-term effects of opioid exposure. Here we review direct neurotoxic, indirect, and stress-related pathophysiologies of prenatal opioid exposure. We describe the literature on short and long-term neurodevelopmental outcomes of children with prenatal opioid exposure, highlighting sex differences and the role of early life stress. We conclude by prioritizing avenues for future research for this group of underserved women and their children at risk for neurodevelopmental delays.

SUBMITTER: Conradt E

PROVIDER: S-EPMC6108075 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature

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Early life stress and environmental influences on the neurodevelopment of children with prenatal opioid exposure.

Conradt Elisabeth E Crowell Sheila E SE Lester Barry M BM

Neurobiology of stress 20180815

Prenatal opioid exposure has reached epidemic proportions. In the last 10 years, there has been a 242% increase in the number of babies born with the drug withdrawal syndrome known as Neonatal Opioid Withdrawal Syndrome (NOWS). Developmental outcome studies of infants with prenatal opioid exposure are limited by methodological issues including small sample sizes and lack of control for confounding variables such as exposure to poverty and maternal psychopathology. Thus, there is a critical gap i ...[more]

PMID: 30151420

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Project description:BackgroundThe association between exposure to secondhand smoke (SHS) during pregnancy and a child's neurodevelopment has not been established yet. We explored the association between prenatal exposure to SHS and neurodevelopment at 24 months of age considering genetic polymorphism and breastfeeding in 720 mothers and their offspring enrolled in the Korean multicenter birth cohort study (Mothers and Children Environmental Health, MOCEH).MethodsWe quantified urine cotinine concentrations in mothers once from 12th to 20th gestational weeks and excluded those whose urine cotinine levels exceeded 42.7 ng/ml to represent SHS exposure in early pregnancy. Mental developmental index (MDI) and psychomotor developmental index (PDI) values were measured using the Korean version of the Bayley Scales of Infant Development II (K-BSID-II) at 24 months of age. A general linear model was used to assess the relationship between maternal urinary cotinine level and neurodevelopment.ResultsMDI scores were inversely associated with cotinine [β = - 2.73; 95% confidence interval (CI): - 5.32 to - 0.15] in children whose mothers had early pregnancy urinary cotinine levels >1.90 ng/ml. No association was evident in children whose mothers had cotinine levels ≤1.90 ng/ml. This negative association was more pronounced in children whose mothers had both Glutathione S-transferases mu 1 (GSTM1) and theta 1 (GSTT1) null type [β = - 5.78; 95% CI: -10.69 to - 0.87], but not in children whose mothers had any present type of GSTM1/GSTT1 [β = - 1.64; 95% CI: -4.79 to 1.52]. The association was no longer significant when children received breast milk exclusively for up to 6 months [β = - 0.24; 95% CI: -4.69 to 4.20] compared to others [β = - 3.75; 95% CI: -7.51 to 0.00]. No significant association was found for PDI.ConclusionsMaternal exposure to SHS during pregnancy may result in delayed MDI in early childhood. This effect might be modified by genetic polymorphism and breastfeeding behavior.

Project description:BackgroundExposure to particulate matter <2.5 μm in diameter (PM2.5) and environmental tobacco smoke (ETS) are associated with respiratory morbidity starting in utero. However, their potential synergistic effects have not been completely elucidated. Here, we examined the joint effects of prenatal and early life PM2.5 and prenatal ETS exposure on respiratory outcomes in children.Material and methodsWe studied 536 mother-child dyads in the Programming Research in Obesity, Growth, Environment and Social Stressors (PROGRESS) study in Mexico City. Exposure to PM2.5 was estimated using residence in pregnancy and child's first year of life with a satellite-based spatio-temporal model. ETS exposure was assessed by caregiver's report of any smoker in the household during the second or third trimester. Outcomes included report of ever wheeze and wheeze in the past 12 months (current wheeze) assessed when children were 6-8 years old considered in separate models. Associations were modeled using distributed lag models (DLM) with daily PM2.5 averages for pregnancy and the first year of life, adjusting for child's sex, birth weight z-score, mother's age and education at enrollment, maternal asthma, season of conception and stratified by prenatal ETS exposure (yes/no).ResultsWe identified a sensitive window from gestational week 14 through postnatal week 18 during which PM2.5 was associated with higher risk of ever wheeze at age 6-8 years. We also observed a critical window of PM2.5 exposure between postnatal weeks 6-39 and higher risk of current wheeze. We found significant associations between higher prenatal and early life PM2.5 exposure and higher cumulative risk ratios of ever wheeze (RR:3.76, 95%CI [1.41, 10.0] per 5 μg/m3) and current wheeze in the past year (RR:7.91, 95%CI [1.5, 41.6] per 5 μg/m3) only among children born to mothers exposed to ETS in pregnancy when compared to mothers who were not exposed.ConclusionsExposure to prenatal ETS modified the association between prenatal and early life PM2.5 exposure and respiratory outcomes at age 6-8 years. It is important to consider concurrent chemical exposures to more comprehensively characterize children's environmental risk. Interventions aimed at decreasing passive smoking might mitigate the effects of ambient air pollution.

Dataset Information

Early life stress and environmental influences on the neurodevelopment of children with prenatal opioid exposure.

Publications

Early life stress and environmental influences on the neurodevelopment of children with prenatal opioid exposure.

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