ABSTRACT
Early temperament, particularly regulation and reactivity, is critical to neurodevelopment and can be shaped by early biological and environmental factors. Prenatal substance exposure is one such influencing factor, often associated with lower regulation and heightened reactivity in infants. However, positive parenting may help mitigate these effects. This study examined how prenatal exposure to alcohol, tobacco, and marijuana influences infant temperament at 24 months, and whether maternal warmth at 12‐ and 24‐months moderates or mediates these relationships. Participants were 404 mother‐child dyads from a prospective, ethnically diverse urban cohort. Results showed prenatal alcohol and tobacco exposure was directly associated with poorer child regulation and reactivity, while marijuana was not independently linked to these outcomes. Maternal warmth at 12 and 24 months moderated some of the negative effects of prenatal tobacco and marijuana exposure, but not alcohol. These moderating effects varied by child outcome, timing, and frequency of substance use. No evidence was found for maternal warmth mediating any of the associations between prenatal substance use and child outcomes. Findings highlight the differential impact of substance type, timing, and frequency on child outcomes and underscore the importance of early parenting support as a resilience factor.
1. Introduction
Early temperament, particularly regulation and reactivity, plays a foundational role in neurocognition (Huizink and Mulder 2006; Toffol et al. 2019; Ursache et al. 2013). Within temperament frameworks, these constructs reflect neurobiologically based individual differences in emotional, attentional, and behavioral responding that are evident early in life and relatively stable over time (Rothbart and Derryberry 1981). Reactivity captures infants' proneness to intense positive or negative emotional responses (e.g., surgency and negative emotionality), whereas regulation reflects attentional and behavioral control processes (Goldsmith 1996; Putnam et al. 2006). Higher regulation in early life is associated with higher executive functioning skills, while heightened reactivity is linked to altered neural pathways in emotion‐related brain regions, such as the amygdala (Bernier et al. 2010; Graham et al. 2016; Filippi et al. 2021; Schwartz et al. 2012; Ursache et al. 2013). Children exposed to substances in utero are at a particularly high risk for developing low regulatory skills and heightened reactivity. Substances such as alcohol, tobacco, and marijuana can cross the placenta and directly impair fetal neurodevelopment, contributing to long‐term challenges in both regulation (Ruisch et al. 2018) and reactivity (Conradt et al. 2018; Locke et al. 2016; Weiss et al. 2007). However, not all children who are exposed prenatally experience negative outcomes (Chu et al. 2022, 2024), suggesting protective factors, such as positive maternal behaviors, may buffer the effects of prenatal substance use on child outcomes (Bergin and McCollough 2009; Jacobson et al. 2004). Alternatively, maternal behaviors may also function as mediators, suggesting prenatal substance use may influence a child's regulatory capacity through negative parenting behaviors (e.g., insensitive, harsh, emotionally unavailable caregiving), that might be correlated with or impacted by substance use (Eiden et al. 2023; Punamäki et al. 2021). Yet, few studies have examined whether specific positive maternal behaviors, such as maternal warmth, act as a mediator and moderator, particularly as it relates to prenatal substance use. This study examines whether maternal warmth, defined by responsiveness and involvement, buffers or exacerbates the effects of prenatal substance exposure on children's temperament, specifically their emotional reactivity and regulation. It also explores whether maternal warmth instead serves as a mediator in the relationship between prenatal substance use and children's temperament. Both pathways were examined because parenting may function either as a mechanism through which prenatal risk is transmitted or as a postnatal resource that modifies children's developmental sensitivity to prenatal exposure.
1.1. Effects of Prenatal Substance Use on Child Regulation and Reactivity
Substance use during pregnancy has been linked to risks for children's neurodevelopment, including the earliest foundations, regulation and reactivity. Variations in the type, frequency, and timing of exposure have been associated with a range of adverse neurodevelopmental and behavioral outcomes in children (Andre et al. 2020; Alvik et al. 2011; Chu et al. 2022; Eiden et al. 2018; Jirikowic et al. 2016; Locke et al. 2016; Ruisch et al. 2018; Terrell et al. 2019). Research indicates prenatal exposure to these substances can impair self‐regulation and stress responses in infants, leading to difficulties in mood, arousal, and behavioral control (Kable et al. 2016; Sutin et al. 2018; Paul et al. 2021; Perry et al. 2024). Higher levels of substance exposure are associated with greater difficulties in emotional regulation and reactivity, whereas lower or sporadic use may lead to different, and sometimes less severe, developmental consequences (Bakhireva et al. 2024; May et al. 2021; McDonald and Watson 2020; O'Connor 2001; Schoeps et al. 2018). Finally, the first trimester exposure is of particular concern, as this period is marked by heightened vulnerability in fetal brain development, making it more susceptible to long‐term temperament‐related challenges (Etemadi‐Aleagha and Akhgari 2022; Singer et al. 2020). Unfortunately, the first trimester is also the time when substance use is most prevalent among pregnant individuals (Genna et al. 2022; Havens et al. 2009; Ko et al. 2015) and therefore, might have unique detrimental impacts compared to continued exposure across all trimesters (Singer et al. 2020). For this reason, the current study examines substance‐specific associations of prenatal alcohol, tobacco, and marijuana exposure with toddler regulation and reactivity, including exploratory analyses of timing (first trimester vs. overall pregnancy) and dose (frequency).
Children with prenatal alcohol exposure often show early difficulties in reactivity and regulation, including heightened irritability, poor emotional control, and negative affect (Alvik et al. 2011; Jirikowic et al. 2016; Lin et al. 2018; O'Connor 2001; Reid and Petrenko 2018; Schoeps et al. 2018). Prenatal alcohol exposure interferes with neurotransmitter functioning and hippocampal development involved in executive functioning and self‐regulation (Connor et al. 2000; Dunty et al. 2001; Mattson et al. 2001; Riley et al. 2004; Zhou et al. 2005). Supporting this, Haley et al. (2006) found infants with higher levels of prenatal alcohol exposure exhibited altered cortisol reactivity and regulation during a modified still‐face paradigm, including blunted or exaggerated responses to stress and delayed recovery, indicative of disrupted hypothalamic–pituitary–adrenal (HPA) axis functioning. Similarly, a systematic review found binge drinking more than once, early in pregnancy (0–6 weeks), was associated with a difficult temperament in infants (6–24 months; Chu et al. 2022). Further emphasizing the role of exposure patterns, Nulman et al. (2004) found frequent binge drinking during the first trimester was linked to distinct temperament traits in children, such as increased approachability, greater adaptability, and reduced distractibility, traits that may reflect underlying regulatory difficulties.
Tobacco use is the most common substance consumed during pregnancy, with prevalence rates as high as 30% (Froggatt et al. 2020b; Sutin et al. 2018). Prenatal exposure to tobacco impairs nutrient exchange and restricts growth which has been linked to a range of adverse neurobehavioral outcomes in infants, including heightened negative affect, reduced attention, increased excitability and irritability, and difficulties with regulation and orientation (Eiden et al. 2018; Froggatt et al. 2020a; Sutin et al. 2018; Wiebe et al. 2014). In a study using four independent samples, Sutin et al. (2018) found children exposed to prenatal tobacco exhibited greater emotional reactivity, lower persistence, and reduced sociability from ages 2 to 12, even after controlling for demographic factors. Similarly, Wiebe et al. (2014) found infants exposed prenatally to tobacco displayed more intense negative reactions during a frustration task and relied more on caregiver cues for emotional regulation, indicating heightened reactivity and altered coping mechanisms. Higher prenatal tobacco exposure, assessed through maternal cotinine levels and reported numbers of cigarettes used, has also been associated with a dose‐response pattern of neurobehavioral difficulties, including increased stress and excitability (Law et al. 2003) and elevated attention problems in infants (Eiden et al. 2018). These associations were strongest with first trimester exposure, likely reflecting both heightened vulnerability during early neurodevelopment and higher substance use during this period (Eiden et al. 2018).
Marijuana is a psychoactive substance often perceived as a harmless recreational drug in many parts of the world, despite increasing evidence it can have harmful effects on the developing brain (Hurd et al. 2019; Jacques et al. 2020; Vishnubhotla et al. 2024). Marijuana use has significantly increased in recent years, with many women continuing to use it during pregnancy (Volkow et al. 2019). Research shows prenatal marijuana exposure can alter brain structure and connectivity of the fetal brain, contributing to downstream problems in children, with effects varying by timing and amount of exposure, as well as the child's age at assessment (Genna et al. 2022; Huizink 2014; Reyentanz et al. 2025). Most recently, a systematic review by Reyentanz et al. (2025) found prenatal marijuana exposure to be associated with decreased self‐soothing and emotional regulation in infants, although these effects were less evident in children over 16 months. Earlier work by Huizink (2014) linked prenatal marijuana exposure to disruptions in early neurobehavioral development, including increased reactivity, high‐pitched crying, hyperirritability, and agitation. Furthermore, Genna et al. (2022) found marijuana exposure during the first trimester of pregnancy, compared to later periods, was associated with an elevated risk of hyperactivity and aggression in infancy and early childhood, behaviors indicative of difficulties with regulation. Together, this research underscores prenatal exposure to alcohol, tobacco, and marijuana, particularly during the first trimester, can impair children's emerging regulatory abilities. However, effects vary substantially by substance type, timing, and exposure pattern, and these substances operate through partially distinct biological and neurodevelopmental mechanisms. Accordingly, the present study focuses on substance‐specific associations with child regulation and reactivity, examining alcohol, tobacco, and marijuana in separate analytic models while exploring variation by timing and frequency of exposure for available data.
1.2. The Role of Parenting
While many early factors may contribute to the development of regulation and reactivity, parenting behaviors play a critical role in shaping early neurodevelopment. Maternal warmth, often expressed through responsiveness (sensitivity to the child's verbal and emotional cues) and involvement (active engagement in the child's activities), supports autonomy and emotional development without compromising the child's sense of self (von Suchodoletz et al. 2011). It also promotes a child's regulation by fostering a secure attachment, which provides children with a sense of safety and security that comfort will be available during times of distress (dos et al. 2020). Importantly, maternal warmth may operate through multiple developmental pathways, functioning either as a mediator or a moderator of the association between prenatal substance exposure and child temperament. From a mediation perspective, prenatal substance use may be associated with subsequent caregiving quality, such that substance‐related stressors or dysregulation may compromise maternal warmth, which in turn shapes children's emerging regulation and reactivity (Guyon‐Harris et al. 2023; Jacques et al. 2020). From a moderation perspective, maternal warmth may instead represent a relatively independent postnatal resource that alters the strength of associations between prenatal exposure and child outcomes, buffering, or in some cases exacerbating, risk regardless of the level of prenatal substance use (Eiden et al. 2023; Hartman et al. 2023). Notably, prior literature has produced mixed and sometimes inconsistent findings regarding whether caregiving functions primarily as a pathway of risk or as a source of resilience in the context of prenatal substance exposure, underscoring the need to explicitly test both mechanisms within a single framework (Hartman et al. 2023; Perry et al. 2024). Considering both pathways allows for a more comprehensive test of how postnatal caregiving may either transmit or attenuate early biological risk.
1.2.1. Maternal Warmth as a Moderator
One way research suggests parenting may influence child outcomes is by buffering children against the effects of earlier adverse environments, such as prenatal substance exposure (Hartman et al. 2023). Eiden et al. (2023) showed sensitive parenting reduced the risk of blunted cortisol reactivity in children with prenatal tobacco exposure, suggesting warm, responsive caregiving can help regulate physiological stress responses in early development. In addition, Elkins (2025) found the negative effects of prenatal substance exposure on toddler temperament, specifically lower surgency and higher negative affect, were attenuated in the presence of higher maternal warmth. Together, these findings point to the potential of parenting, particularly maternal warmth, as a protective factor that can moderate the negative effects of prenatal substance exposure.
1.2.2. Maternal Warmth as a Mediator
Parenting may also serve as a mediator of the effects of prenatal substance use on child regulation and reactivity (see Peisch et al. 2018 for a review). Substance use during pregnancy has been associated with increased risk for challenges in postnatal parenting, including lower responsiveness, increased irritability, or inconsistency in caregiving (Guyon‐Harris et al. 2023; Jacques et al. 2020; Mayes and Truman 2002). For instance, Schuetze et al. (2019) reported prenatal exposure to tobacco and marijuana predicted higher maternal anger and hostility in infancy, which then contributed to poorer autonomic regulation in toddlers at 16 months. Notably, the direct effect of prenatal exposure on toddler regulation was minimal, suggesting early caregiving behaviors were a key mechanism of transmission. Punamäki et al. (2021) similarly demonstrated early maternal emotional availability mediated the association between prenatal substance use (i.e., marijuana) and later emotion dysregulation in children. These findings highlight that the postnatal parenting environment may reflect the same vulnerabilities present in the prenatal environment, compounding early risk and contributing to escalating challenges in early regulation and reactivity.
1.3. Present Study
Prenatal exposure to alcohol, tobacco, and marijuana has been linked to disruptions in child temperament and neurodevelopment; given their distinct mechanisms and patterns of co‐use, substance‐specific analyses are needed to disentangle their associations with early regulation and reactivity. In addition, although the literature is limited, emerging research has explored maternal parenting as a moderator or mediator of child regulation and reactivity in the context of prenatal substance exposure. However, few studies have examined both pathways within the same study, limiting our understanding of how parenting might influence child temperament in the context of prenatal substance exposure. Prior findings suggest prenatal substance use may negatively impact the quality of postnatal maternal care, while other studies indicate positive parenting may buffer the effects of a substance‐exposed prenatal environment (Eiden et al. 2023; Elkins 2025; Perry et al. 2024; Schuetze et al. 2019). In the present study, we examine both the mediating and moderating effects of maternal parenting, specifically maternal warmth, in shaping regulation and reactivity among 24‐month‐old children. Exploratorily, we re‐estimated all primary models using alternative operationalizations of prenatal substance use (alcohol and tobacco only), including overall pregnancy exposure versus first‐trimester use, and binary indicators of use versus frequency of use. Guided by this literature and conceptual framework, we tested the following hypotheses:
Hypothesis 1
In substance‐specific models, higher levels of prenatal substance use (alcohol, tobacco, and marijuana) will be associated with child regulation and reactivity at 24 months of age. Specifically, prenatal alcohol exposure will be associated with higher emotional reactivity, tobacco exposure with lower regulatory processes, and prenatal marijuana exposure with lower regulation and higher reactivity.
Hypothesis 2
Maternal warmth at 12 and 24 months will buffer the associations between prenatal substance exposure (alcohol, tobacco, or marijuana) and child regulation and reactivity at 24 months.
Hypothesis 3
Maternal warmth will mediate the association between prenatal substance use (alcohol, tobacco, or marijuana) and child regulation and reactivity at 24 months. Specifically, higher levels of prenatal substance use will be associated with lower levels of maternal warmth, which in turn will be associated with greater child reactivity and poorer regulation.
Exploratory Hypotheses: In addition to these primary hypotheses, we conducted exploratory analyses within the same substance‐specific modeling framework to examine whether associations between prenatal substance exposure, maternal warmth, and child outcomes differed based on how prenatal substance use was operationalized. Specifically, we re‐estimated analyses using alternative operationalizations of prenatal substance exposure, including (a) first‐trimester‐only use and (b) frequency of use for alcohol and tobacco (frequency data were unavailable for marijuana).
2. Methods
2.1. Participants and Procedures
Data were obtained from a prospective longitudinal study following mother‐child dyads beginning in the mothers' third trimester of pregnancy and continuing until their children were between 7 and 9 years old. Participants were recruited as part of the Mount Sinai Children's Environmental Health Study, a longitudinal birth cohort conducted in New York City (Engel et al. 2007). The original cohort included a diverse sample of primiparous women with singleton pregnancies. Seventy‐five women were excluded for reasons detailed elsewhere (Engel et al. 2007), including extreme prematurity, resulting in a final cohort of 404 women for whom birth data were available. Pregnant participants provided written informed consent prior to their participation in the study, including consent for the use of information related to their future babies. The current study was approved by the Utah State University Institutional Review Board #15286.
On average, mothers in the sample were approximately 24 years old. The sample was 20% White, 28% Black, and 51% Hispanic or from another racial/ethnic background. Among the children, 54% were identified as male and 46% as female. Full demographic characteristics of the overall sample are presented in Supporting Information S1: Table S1 presents demographic characteristics for the subsample used in the present study, those who reported use of at least one substance (alcohol, tobacco, or marijuana) and who completed at least one subscale of the child temperament measure. Data were analyzed from three time points: the third trimester of pregnancy (25–40 weeks, Time 1 ), when the child was 12 months old (Time 2 ), and when the child was 24 months old (Time 3 ). Participation varied across time points, with 404 total participants at Time 1 , 204 (50%) dyads at Time 2 , and 279 dyads (69.1%) at Time 3 .
2.2. Attrition and Missing Data
Some mother‐child dyads were lost to follow‐up due to non‐response, refusals to continue participation, or challenges related to relocation, resulting in 204 dyads at Time 2 and 278 dyads at Time 3 . An analysis of attrition revealed most demographic variables did not significantly differ between those who presented for follow‐up, and those who did not. However, mothers who participated at Time 2 were older than those who did not participate (24.43 years old vs. 22.71 years old). Additionally, mothers with lower education levels, were more likely to not participate at Time 3 compared to mothers who did participate.
2.3. Measures
2.3.1. Prenatal Substance Use
Prenatal substance use focused on different substances: (a) alcohol, (b) tobacco, and (c) marijuana. Participants were asked if they did or did not use any of the substances prenatally. For mothers who drank alcohol, they were asked about their weekly intake of various types of alcohol, including wine, beer, and liquor, during each trimester (first, second, and/or third). The questionnaire assessed the number of glasses or bottles consumed per week for each type of alcohol across the three trimesters. For mothers who indicated they smoked tobacco, they were asked how many cigarettes they smoked daily in each trimester (first, second, and/or third). Because data collection occurred during the third trimester of pregnancy, mothers reported on their substance use during the first and second trimesters retrospectively. For marijuana, mothers responded with a simple ‘yes’ or ‘no’ to indicate use during pregnancy and there were no questions regarding dosage.
2.3.2. Child Regulation and Reactivity
Child regulation and reactivity were assessed using the Toddler Behavior Assessment Questionnaire (TBAQ; Goldsmith 1996) when the child was approximately 24 months old. Mothers completed an assessment consisting of five content scales. Higher scores on the activity scale (α = 0.78) reflect greater movement. The anger scale (α = 0.82) indicates a higher tendency to cry or protest during conflict. The social fear scale (α = 0.83) measures inhibition or withdrawal in new social situations. The interest scale (α = 0.79) assesses the amount of time spent in independent play. Finally, the pleasure scale (α = 0.80) evaluates smiling, laughing, and positive vocal communication.
2.3.3. Maternal Warmth
The quality of children's home environment was assessed using the Home Observation for Measurement of the Environment (HOME) inventory (Caldwell and Bradley 1984). The HOME inventory was administered during the 12‐ and 24‐month visits through an in‐home interview while the child was present, incorporating both maternal reports and observer ratings. This study focused on two subscales of the HOME inventory: involvement and responsivity. The involvement subscale assesses how an adult physically interacts with the child. The responsivity subscale measures the emotional and verbal sensitivity of the parent to the child. The involvement and responsivity subscales were highly correlated (r = 0.49, p < 0.001) and were therefore combined into a single composite variable.
2.3.4. Covariates
We included maternal age, race/ethnicity, and child sex as covariates in the main analyses. Maternal age was included as a covariate because mothers who participated at Time 2 were significantly older than those who did not (24.43 vs. 22.71 years), potentially influencing study retention and child outcomes. Maternal race has been shown to be associated with both prenatal substance use and child developmental outcomes. Child sex was included because males and female infants differ in emotion regulation and reactivity, and vulnerability to early adversity during early life (El Marroun et al. 2011).
2.4. Analytic Strategy
All analyses, including correlations and regression analyses, were conducted using R version 4.4.1 with the following packages: regtools 1.7.0, mediation 4.5.0, laavan 0.6–19, broom 1.0.6, and dplyr 1.1.4. Missingness in the analytic sample was primarily due to attrition across study waves. Attrition analyses indicated no differences in missingness by child sex (e.g., χ 2 ≤ 0.51, p ≥ 0.47), marital status (e.g., χ 2 ≤ 4.12, p ≥ 0.13), maternal race/ethnicity (e.g., Fisher's exact test p ≥ 0.14), breastfeeding status (e.g., χ 2 ≤ 2.27, p ≥ 0.13), or prenatal substance exposure (alcohol, tobacco, or marijuana; e.g., χ 2 ≤ 1.84, p ≥ 0.18). In contrast, mothers with missing child temperament data were consistently younger than those retained across outcomes (e.g., t = −2.43 to −3.50, p ≤ 0.02). Maternal education was associated with missingness for one temperament outcome (social fear; χ 2(3) = 8.25, p = 0.04). Accordingly, maternal age and education were included as covariates, and sensitivity analyses incorporating additional sociodemographic variables (i.e., maternal race, marital status, and residence type) yielded substantively similar results (see Supporting Information S1: Tables S8–S19).
Assumptions for all regression‐based analyses were evaluated prior to hypothesis testing. Linearity, homoscedasticity, and residual normality were assessed using standard diagnostic plots (residuals‐versus‐fitted, scale–location, and Q–Q plots), which indicated no meaningful violations. Multicollinearity was low (all VIFs < 2.5; O’Brien 2007), and influence diagnostics showed no observations exceeding Cook's distance thresholds (Cook 1977).
2.4.1. Primary Hypotheses
Each hypothesis was tested in substance‐specific models (alcohol, tobacco, marijuana) for each temperament outcome (i.e., anger, social fear, interest, pleasure, activity levels); thus, estimates reflect associations for each substance examined separately rather than mutually adjusted effects. To test Hypothesis 1, we examined whether prenatal exposure to alcohol, tobacco, and marijuana (Time1) was associated with child emotional reactivity and regulation at 24 months of age (Time 3 ). Hypothesis 1 focused on the direct associations between prenatal substance exposure and child outcomes, which were estimated within both moderation and mediation models to allow consistent comparison across analytic frameworks. Direct effects were first estimated in moderation models using multiple linear regression, in which prenatal substance exposure was entered as a predictor of child outcomes while maternal warmth and demographic covariates were included as controls. Direct effects were also estimated in mediation models using structural equation modeling, representing associations between prenatal substance exposure and child outcomes after accounting for indirect effects through maternal warmth. Structural equation modeling further decomposed total effects into direct and indirect components, which may differ from estimates obtained in regression‐based moderation models. Despite these methodological differences, results across approaches were largely consistent.
We tested Hypothesis 2, that maternal warmth at 12 and 24 months (Time 2 and Time 3 ) would moderate the associations between prenatal substance use and child outcomes, using multiple linear regression models. Separate substance‐specific models were estimated for maternal warmth at each time point. Interaction terms between prenatal substance exposure and mean‐centered maternal warmth were included to assess moderation, with demographic covariates (maternal age, maternal race/ethnicity, and child sex) entered in all models. For significant interaction effects (p < 0.05), conditional associations between prenatal substance use and child outcomes were examined using post‐hoc probing. Simple slopes were estimated at low (−1 SD), mean, and high (+1 SD) levels of maternal warmth, and Johnson–Neyman intervals were used to identify regions of maternal warmth for which prenatal substance exposure was significantly associated with child outcomes. Interaction patterns were visualized to aid interpretation of the direction and magnitude of effects.
To assess Hypothesis 3, that maternal warmth mediates the association between prenatal substance use and child outcomes, mediation analyses were conducted within a structural equation modeling framework using a product‐of‐coefficients approach (Hayes and Preacher 2013). Indirect effects were estimated by modeling the association between prenatal substance use and maternal warmth (path a) and the association between maternal warmth and child regulation and reactivity at 24 months while controlling for prenatal substance use (path b), with the indirect effect quantified as the product of these paths (a × b). Indirect effects were evaluated using bias‐corrected bootstrapped confidence intervals based on 5000 resamples to account for non‐normality in the sampling distribution of indirect effects (Hayes and Preacher 2013; Preacher and Hayes 2008). Mediation was considered supported when the 95% confidence interval for the indirect effect did not include zero. Model adequacy was evaluated using multiple complementary fit indices, including the chi‐square test of model fit (χ 2), the comparative fit index (CFI), the Tucker–Lewis index (TLI), the root mean square error of approximation (RMSEA), and the standardized root mean square residual (SRMR). Following established recommendations (Hu and Bentler 1998; Schermelleh‐Engel et al. 2003), acceptable model fit was indicated by at least three of the five fit indices being above established guidelines as indicated by a nonsignificant χ 2 test, RMSEA values ≤ 0.08, SRMR values ≤ 0.08, and CFI/TLI values ≥ 0.90. Standardized coefficients were extracted to evaluate the magnitude of direct, indirect, and total effects.
2.4.2. Exploratory Analyses: Timing and Dose
Given prior evidence indicating the first trimester represents both a critical period for fetal neurodevelopment and the most common period for prenatal substance use (Etemadi‐Aleagha and Akhgari 2022; Singer et al. 2020), we conducted exploratory analyses to examine whether associations among prenatal substance exposure, maternal warmth, and child outcomes differed based on timing of exposure. To do so, the moderation and mediation models described for Hypotheses 1–3 were re‐estimated using first‐trimester substance use in place of overall pregnancy exposure; trimester‐specific analyses beyond the first trimester were not conducted due to limited data. Additional exploratory models examined frequency of use for alcohol and tobacco by substituting continuous measures (drinks per week; cigarettes per day) for binary exposure indicators. Frequency‐ and timing‐based analyses were not conducted for marijuana due to data limitations.
2.4.3. Sensitivity Analysis
As a sensitivity analysis, we repeated the analysis with additional covariates, including maternal education, marital status, and residence type, that also might be related to parenting style, environmental stability, and mother‐child well‐being (Weis et al. 2022). The results from these additional analyses are presented in Supporting Information S1: Tables S8–S19.
3. Results
In the sections below, results are organized according to the primary hypotheses. Within each hypothesis, exploratory analyses examining alternative operationalizations of prenatal substance exposure (timing and frequency) are explicitly noted.
3.1. Descriptive Statistics and Bivariate Correlations
A total of 28.3% of participants reported prenatal use of at least one substance (alcohol, tobacco, or marijuana) and had data available for at least one child temperament subscale at 24 months (Table 1). Overall alcohol use was significantly negatively correlated with child interest (r = −0.13, p < 0.05) and child activity (r = −0.14, p < 0.05). The frequency of prenatal tobacco use was negatively correlated with child interest (r = −0.15, p < 0.05). Parental warmth at 24 months was modestly negatively correlated with child activity (r = −0.13, p < 0.05). Correlations between key variables in the study are displayed in Table 2.
TABLE 1.
Participant demographic characteristics by substance use (alcohol, tobacco, marijuana).
|
Participant characteristics (n) |
Alcohol use | Tobacco use | Marijuana use | |||
|---|---|---|---|---|---|---|
| Yes | No | Yes | No | Yes | No | |
| Maternal race/ethnicity | ||||||
| Non‐Hispanic White | 17 | 46 | 5 | 59 | 0 | 64 |
| Black | 8 | 63 | 14 | 59 | 6 | 67 |
| Hispanic | 13 | 122 | 25 | 114 | 10 | 129 |
| Other | 0 | < 5 | < 5 | < 5 | < 5 | < 5 |
| Maternal education | ||||||
| < High school | < 5 | 70 | 14 | 65 | 6 | 73 |
| High school | < 5 | 51 | 10 | 45 | 6 | 49 |
| Some college | 11 | 58 | 13 | 56 | 5 | 64 |
| ≥ College degree | 20 | 55 | 8 | 68 | 0 | 76 |
| Child's sex | ||||||
| Male | 20 | 127 | 26 | 125 | 9 | 142 |
| Female | 18 | 107 | 19 | 109 | 8 | 120 |
| Maternal age | ||||||
| < 20 years | 7 | 82 | 12 | 82 | 10 | 84 |
| 20 < 30 years | 15 | 104 | 22 | 98 | 7 | 113 |
| 30+ years | 16 | 48 | 11 | 54 | 0 | 65 |
| Marital status | ||||||
| Married | 16 | 66 | 7 | 76 | 0 | 83 |
| Living with father of child | 6 | 53 | 8 | 53 | 5 | 56 |
| Single/Divorced/Widowed | 16 | 115 | 30 | 105 | 12 | 123 |
| Residence type | ||||||
| High‐rise apartment (> 8 stories) | 13 | 103 | 21 | 100 | 5 | 116 |
| Small apartment (≤ 7 stories) | 18 | 108 | 21 | 107 | 10 | 118 |
| Private home | 6 | 22 | < 5 | 25 | < 5 | 26 |
Note: Values represent counts of participants reporting “Yes” or “No” use of alcohol, tobacco, or marijuana during pregnancy, stratified by demographic characteristics. Cell counts < 5 were suppressed to protect participant confidentiality.
TABLE 2.
Pearson's correlations for prenatal substance use, maternal and child demographics, child regulation and reactivity outcomes at 24 months, and parental warmth at 12 and 24 months.
| Variable | M | SD | 1 | 2 | 3 | 4 | 5 | 6 | 7 | 8 | 9 | 10 | 11 | 12 | 13 |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 1. Overall alcohol | 0.15 | 0.36 | |||||||||||||
| 2. 1st Trim alcohol | 0.28 | 1.05 | 0.63** | ||||||||||||
| 3. Frequency of alcohol | 0.37 | 1.25 | 0.71** | 0.88** | |||||||||||
| 4. Overall tobacco | 0.17 | 0.37 | 0.08 | 0.14** | 0.13** | ||||||||||
| 5. 1st trim tobacco | 0.83 | 2.64 | 0.04 | 0.15** | 0.11* | 0.70** | |||||||||
| 6. Frequency of tobacco | 1.23 | 4.63 | 0.01 | 0.12* | 0.09 | 0.60** | 0.88** | ||||||||
| 7. Overall marijuana | 0.05 | 0.22 | 0.07 | 0.10 | 0.07 | 0.27 | 0.26 | 0.17 | |||||||
| 8. Warmth 12 mos | 6.77 | 0.84 | −0.07 | −0.12 | −0.08 | −0.07 | −0.08 | −0.05 | −0.02 | ||||||
| 9. Warmth 24 mos | 7.15 | 1.90 | −0.01 | −0.05 | 0 | −0.06 | −0.06 | −0.08 | 0.05 | 0.12 | |||||
| 10. Child anger | 4.04 | 1.88 | −0.04 | 0.01 | −0.03 | −0.02 | −0.11 | −0.12 | −0.05 | −0.06 | −0.10 | ||||
| 11. Child social fear | 4.16 | 0.97 | −0.01 | −0.05 | −0.09 | −0.09 | −0.07 | −0.05 | −0.05 | 0.00 | −0.03 | 0.16 | |||
| 12. Child interest | 4.86 | 0.76 | −0.13* | −0.03 | −0.02 | −0.06 | −0.05 | −0.15* | −0.02 | −0.07 | 0.12 | −0.15* | −0.07 | ||
| 13. Child pleasure | 5.73 | 0.64 | −0.09 | −0.01 | −0.08 | 0 | −0.02 | −0.10 | 0.02 | 0.05 | 0.09 | 0.04 | −0.26** | 0.31** | |
| 14. Child activity | 4.45 | 0.84 | −0.14 | −0.07 | −0.12 | 0.01 | −0.05 | −0.05 | −0.06 | −0.06 | −0.13* | 0.54** | 0.03 | −0.18** | 0.14* |
Note: Bold values indicate statistically significant results. *p < 0.05. **p < 0.01.
3.2. The Relationship Between Prenatal Substance Use and Child Regulation and Reactivity (Hypothesis 1)
Direct effects of prenatal substance use on child regulation and reactivity can be found in the moderation Tables 3, 4, 5, 6, 7, 8. Alcohol use during pregnancy was negatively associated with child interest (β = −0.29, 95% CI [−0.57, −0.01]), but not with anger, pleasure, social fear, or activity level (all p > 0.05). When alcohol exposure was examined based on 1st‐trimester‐only use or frequency of use, no significant associations with any child outcomes were found. These results are detailed in Tables 3, 4, 5, 6, 7, 8. In contrast, tobacco use showed more consistent associations. Regardless of how it was operationalized, overall use (β = −0.46, 95% CI [−0.75, −0.16]), 1st trimester use (β = −0.05, 95% CI [−0.10, −0.01]), or frequency of use (β = −0.04, 95% CI [−0.06, −0.02]), tobacco exposure was negatively associated with child interest. It was also negatively associated with child pleasure across all three tobacco use indicators: overall use (β = −0.37, 95% CI [−0.72, −0.02]), 1st trimester use (β = −0.05, 95% CI [−0.10, 0.00]), and frequency (β = −0.02, 95% CI [−0.04, −0.01]). Additionally, first‐trimester tobacco exposure (β = −0.04, 95% CI [−0.08, 0.00]) and frequency of tobacco use (β = −0.02, 95% CI [−0.04, 0.00]) were each associated with lower child anger. However, tobacco use was not significantly related to child social fear or activity level (all p > 0.05). These findings can be found in Tables 3, 4, 5, 6, 7, 8. Marijuana exposure during pregnancy was not significantly associated with most child outcomes; however, prenatal marijuana exposure was negatively associated with child interest (β = −0.39, 95% CI [−0.73, −0.04]; Tables 7 and 8).
TABLE 3.
Hierarchical linear regression of child outcomes, prenatal alcohol exposure, and maternal warmth measured at 12 Months as a moderator.
| Step | Anger | Social fear | Interest | Pleasure | Activity |
|---|---|---|---|---|---|
| 1. Controls | |||||
| Mother's age | −0.01 [−0.04, 0.01] | −0.02 [−0.05, 0.00] | 0.00 [−0.02, 0.01] | −0.01 [−0.03, 0.00] | −0.03 [−0.05, 0.00] |
| Child's sex | 0.18 [−0.10, 0.45] | −0.01 [−0.32, 0.30] | −0.04 [−0.28, 0.19] | 0.02 [−0.18, 0.22] | 0.03 [−0.22, 0.28] |
| Maternal race | 0.07 [−0.10, 0.24] | −0.08 [−0.27, 0.11] | 0.04 [−0.11, 0.18] | 0.08 [−0.05, 0.20] | −0.01 [−0.17, 0.14] |
| 2. Main effects | |||||
| Alcohol | 0.05 [−0.36, 0.46] | 0.32 [−0.14, 0.77] | −0.34* [−0.68, 0.00] | −0.04 [−0.35, 0.26] | −0.25 [−0.63, 0.12] |
| 1st trim alcohol | −0.04 [−0.24, −0.14] | 0.06 [−0.14, 0.26] | −0.04 [−0.19, 0.11] | 0.05 [−0.08, 0.18] | 0.00 [−0.20, 0.13] |
| Frequency | −0.02 [−0.14, 0.10] | 0.00 [−0.12, 0.13] | 0.01 [−0.09, 0.10] | 0.00 [−0.08, 0.08] | −0.06 [−0.16, 0.05] |
| 3. Main Effects | |||||
| Warmth 12 mos | −0.02 [−0.21, 0.17] | 0.12 [−0.11, 0.33] | 0.00 [−0.27, 0.06] | 0.00 [−0.14, 0.14] | −0.05 [−0.22, 0.13] |
| 4. Interaction effects | |||||
| Alcohol × Warmth 12 mos | 0.00 [−0.42, 0.42] | −0.15 [−0.60, 0.31] | 0.07 [−0.29, 0.42] | 0.18 [−0.13, 0.48] | 0.03 [−0.35, 0.40] |
| 1st trim × Warmth 12 mos | −0.09 [−0.26, 0.07] | 0.03 [−0.12, 0.18] | 0.04 [−0.07, 0.16] | 0.08 [−0.02, 0.18] | 0.00 [−0.11, 0.13] |
| Frequency × Warmth 12 mos | −0.03 [−0.16, 0.10] | −0.01 [−0.12, 0.10] | 0.07 [−0.02, 0.15] | 0.05 [−0.02, 0.13] | 0.00 [−0.10, 0.09] |
Note: Alcohol = Any alcohol use during pregnancy (yes/no). 1st Trim Alcohol = Alcohol consumed only in the first trimester. Frequency = Amount of alcohol consumed throughout the entire pregnancy. Bold values indicate statistically significant results. *p < 0.05. **p < 0.01.
TABLE 4.
Hierarchical linear regression of child outcomes, prenatal alcohol exposure, and maternal warmth measured at 24 Months as a moderator.
| Step | Anger | Social fear | Interest | Pleasure | Activity |
|---|---|---|---|---|---|
| 1. Controls | |||||
| Mother's age | 0.00 [−0.03, 0.01] | −0.03** [−0.05, −0.01] | 0.00 [−0.02, 0.01] | −0.01 [−0.02, 0.00] | −0.02 [−0.04, 0.00] |
| Child's sex | 0.18 [−0.04, 0.40] | 0.12 [−0.12, 0.36] | 0.05 [−0.14, 0.24] | −0.02 [−0.18, 0.13] | 0.05 [−0.15, 0.25] |
| Maternal race | 0.12 [−0.03, 0.26] | −0.07 [−0.24, 0.09] | 0.08 [−0.04, 0.20] | 0.08 [−0.02. 0.18] | 0.05 [−0.08, 0.18] |
| 2. Main Effects | |||||
| Alcohol | 0.00 [−0.33, 0.32] | 0.05 [−0.29, 0.40] | −0.29 [−0.57, −0.01] | −0.07 [−0.31, 0.16] | −0.24 [−0.53, 0.05] |
| 1st Trim alcohol | 0.00 [−0.14, 0.15] | −0.05 [−0.18, 0.08] | −0.01 [−0.12, 0.09] | 0.00 [−0.09, 0.09] | −0.07 [−0.19, 0.40] |
| Frequency | 0.00 [−0.10, 0.10] | −0.05 [−0.14, 0.05] | −0.01 [−0.09, 0.07] | −0.03 [−0.09, 0.04] | −0.06 [−0.14, 0.02] |
| 3. Main Effects | |||||
| Warmth 24 mos | −0.04 [−0.19, 0.10] | 0.03 [−0.12, 0.19] | 0.09 [−0.03, 0.22] | 0.08 [−0.02, 0.18] | −0.10 [−0.22, 0.03] |
| 4. Interaction Effects | |||||
| Alcohol × Warmth 24 mos | −0.16 [−0.55, 0.23] | −0.18 [−0.59, 0.22] | 0.30 [−0.11, 0.72] | −0.12 [−0.47, 0.22] | 0.00 [−0.32, 0.33] |
| 1st Trim × Warmth 24 mos | −0.03 [−0.13, 0.07] | −0.02 [−0.12, 0.08] | 0.04 [−0.09, 0.16] | 0.02 [−0.09, 0.13] | −0.02 [−0.11, 0.06] |
| Frequency × Warmth 24 mos | −0.03 [−0.12, 0.06] | −0.02 [−0.11, 0.07] | 0.05 [−0.06, 0.15] | −0.02 [−0.10, 0.07] | −0.01 [−0.08, 0.07] |
Note: Alcohol = Any alcohol use during pregnancy (yes/no). 1st Trim Alcohol = Alcohol consumed only in the first trimester. Frequency = Amount of alcohol consumed throughout the entire pregnancy. Bold values indicate statistically significant results. *p < 0.05. **p < 0.01.
TABLE 5.
Hierarchical linear regression of child outcomes, prenatal tobacco exposure, and maternal warmth measured at 12 Months as a moderator.
| Step | Anger | Social fear | Interest | Pleasure | Activity |
|---|---|---|---|---|---|
| 1. Controls | |||||
| Mother's age | −0.02 [−0.04, 0.00] | −0.03 [−0.05, 0.00] | 0.00 [−0.02, 0.02] | −0.01 [−0.03, 0.00] | −0.03** [−0.06, −0.01] |
| Child's sex | 0.19 [−0.08, 0.46] | 0.00 [−0.31, 0.31] | −0.08 [−0.30, 0.14] | 0.00 [−0.19, 0.19] | 0.03 [−0.21, 0.28] |
| Maternal race | 0.08 [−0.10, 0.25] | −0.11 [−0.31, 0.08] | 0.11 [−0.03, 0.25] | 0.10 [−0.02, 0.23] | −0.01 [−0.17, 0.14] |
| 2. Main effects | |||||
| Tobacco | −0.09 [−0.39, 0.22] | −0.06 [−0.66, 0.54] | −0.46** [−0.75, −0.16] | −0.37 [−0.72, −0.02] | −0.14 [−0.59, 0.31] |
| 1st trim tobacco | −0.04 [−0.10, 0.02] | 0.06 [−0.01, 0.12] | −0.05** [−0.10, −0.01] | −0.05* [−0.10, 0.00] | −0.01 [−0.06, 0.04] |
| 3. Main effects | |||||
| Frequency | −0.02 [−0.04, 0.01] | 0.02 [−0.01, 0.05] | −0.04** [−0.06, −0.02] | −0.02 [−0.04, −0.01] | 0.00 [−0.02, 0.02] |
| Warmth 12 mos | −0.09 [−0.27, 0.10] | −0.03 [−0.24, 0.18] | −0.10 [−0.25, 0.05] | 0.05 [−0.08, 0.18] | −0.09 [−0.26, 0.08] |
| 4. Interaction effects | |||||
| Tobacco × Warmth 12 mos | 0.23 [−0.27, 0.73] | 0.35 [−0.20, 0.90] | 0.14 [−0.24, 0.51] | 0.02 [−0.31, 0.35] | 0.34 [−0.09, 0.77] |
| 1st Trim × Warmth 12 mos | 0.01 [−0.10, 0.12] | 0.04 [−0.05, 0.14] | 0.05 [−0.02, 0.11] | 0.01 [−0.04, 0.07] | 0.05 [−0.03, 0.12] |
| Frequency × Warmth 12 mos | 0.00 [−0.07, 0.07] | 0.01 [−0.04, 0.07] | 0.01 [−0.03, 0.04] | 0.00 [−0.03, 0.03] | 0.05* [0.00, 0.09] |
Note: Tobacco = Any tobacco use during pregnancy (yes/no). 1st Trim Tobacco = Tobacco consumed only in the first trimester. Frequency = Amount of tobacco consumed throughout the entire pregnancy. Bold values indicate statistically significant results. *p < 0.05. **p < 0.01.
TABLE 6.
Hierarchical linear regression of child outcomes, prenatal tobacco exposure, and maternal warmth measured at 24 Months as a moderator.
| Step | Anger | Social fear | Interest | Pleasure | Activity |
|---|---|---|---|---|---|
| 1. Controls | |||||
| Mother's age | −0.01 [−0.03, 0.01] | −0.03* [−0.05, 0.00] | 0.00 [−0.02, 0.01] | 0.00 [−0.02, 0.00] | −0.02* [−0.04, 0.00] |
| Child's sex | 0.19* [−0.03, 0.41] | 0.09 [−0.15, 0.33] | 0.03 [−0.16, 0.22] | −0.03 [−0.18, 0.12] | 0.06 [−0.13, 0.26] |
| Maternal race | 0.12 [−0.03, 0.26] | −0.05 [−0.21, 0.12] | 0.10 [−0.02, 0.23] | 0.08 [−0.02, 0.18] | 0.04 [−0.09, 0.18] |
| 2. Main effects | |||||
| Tobacco | −0.09 [−0.39, 0.22] | −0.22 [−0.69, 5.71] | −0.14 [−0.40, 0.12] | −0.13 [−0.42, 0.15] | 0.07 [−0.30, 0.44] |
| 1st trim tobacco | −0.04* [−0.08, 0.00] | −0.02 [−0.07, 0.02] | −0.01 [−0.05, 0.02] | −0.01 [−0.04, 0.02] | −0.02 [−0.05, 0.02] |
| Frequency | −0.02 [−0.04, 0.00] | −0.02 [−1, −0.04] | −0.02 [−0.04, 0.00] | 0.00 [−0.02, 0.01] | 0.07 [0.00, 0.13] |
| 3. Main effects | |||||
| Warmth 24 mos | −0.12 [−0.27, 0.02] | 0.03 [−0.13, 0.18] | 0.14* [0.01, 0.27] | 0.05 [−0.05, 0.16] | −0.01 [−0.03, 0.01] |
| 4. Interaction effects | |||||
| Tobacco × Warmth 24 mos | 0.16 [−0.18, 0.50] | −0.27 [−0.64, 0.09] | −0.12 [−0.40, 0.16] | 0.10 [−0.14, 0.34] | 0.23 [−0.07, 0.53] |
| 1st Trim × Warmth 24 mos | 0.02 [−0.02, 0.07] | −0.05* [−0.10, 0.00] | 0.00 [−0.04, 0.04] | 0.02 [−0.01, 0.06] | 0.02 [−0.02, 0.06] |
| Frequency × Warmth 24 mos | 0.01 [−0.02, 0.04] | −0.04* [−0.08, 0.00] | 0.01 [−0.02, 0.04] | 0.02* [0.00, 0.05] | 0.00 [−0.03, 0.03] |
Note: Tobacco = Any tobacco use during pregnancy (yes/no). 1st Trim Tobacco = Tobacco consumed only in the first trimester. Frequency = Amount of tobacco consumed throughout the entire pregnancy. Bold values indicate statistically significant result. *p < 0.05. **p < 0.01.
TABLE 7.
Hierarchical linear regression of child outcomes, prenatal marijuana exposure, and maternal warmth measured at 12 Months as a moderator.
| Step | Anger | Social fear | Interest | Pleasure | Activity |
|---|---|---|---|---|---|
| 1. Controls | |||||
| Mother's age | −0.02 [−0.04, 0.00] | −0.03* [−0.05, 0.00] | −0.01 [−0.03, 0.01] | −0.01 [−0.04, 0.00] | −0.03** [−0.05, −0.01] |
| Child's sex | 0.17 [−0.10, 0.45] | 0.01 [−0.29, 0.32] | −0.09 [−0.31, 0.12] | 0.00 [−0.20, 0.19] | 0.04 [−0.20, 0.29] |
| Maternal race | 0.07 [−0.10, 0.24] | −0.09 [−0.28, 0.11] | 0.08 [−0.06, 0.22] | 0.10 [−0.02, 0.23] | −0.01 [−0.17, 0.14] |
| 2. Main Effects | |||||
| Marijuana | −0.09 [−0.73, 0.56] | −0.54 [−1.31, 0.22] | −0.39 [−0.91, 0.14] | −0.07 [−0.52, 0.39] | −0.02 [−0.61, 0.57] |
| Warmth 12 mos | −0.04 [−0.21, 0.13] | 0.02 [−0.17, 0.21] | −0.06 [−0.21, 0.08] | 0.06 [−0.06, 0.18] | −0.04 [−0.20, 0.12] |
| 4. Interaction Effects | |||||
| Marijuana × Warmth 12 mos | −0.64 [−2.08, 0.81] | −0.20 [−1.96, 1.56] | −0.04 [−1.22, 1.13] | −0.66 [−1.68, 0.36] | 0.07 [−1.25, 1.40] |
Note: Marijuana = Any marijuana use during pregnancy (yes/no). Bold values indicate statistically significant results. *p < 0.05. **p < 0.01.
TABLE 8.
Hierarchical linear regression of child outcomes, prenatal marijuana exposure, and maternal warmth measured at 24 Months as a moderator.
| Step | Anger | Social fear | Interest | Pleasure | Activity |
|---|---|---|---|---|---|
| 1. Controls | |||||
| Mother's age | −0.01 [−0.03, 0.01] | −0.03** [−0.05, 0.00] | −0.01 [−0.02, 0.01] | −0.01 [−0.02, 0.00] | −0.02** [−0.04, 0.00] |
| Child's sex | 0.18 [−0.04, 0.40] | 0.11 [−0.13, 0.34] | 0.03 [−0.16, 0.21] | −0.03 [−0.18, 0.12] | 0.07 [−0.13, 0.26] |
| Maternal race | 0.12 [−0.02, 0.27] | −0.06 [−0.23, 0.10] | 0.09 [−0.03, 0.21] | 0.09 [−0.01, 0.19] | 0.06 [−0.07, 0.19] |
| 2. Main Effects | |||||
| Marijuana | −0.25 [−0.71, 0.22] | −0.31 [−0.85, 0.22] | −0.08 [−0.48, 0.32] | −0.03 [−0.36, 0.30] | −0.40 [−0.81, 0.02] |
| 3. Main Effects | |||||
| Warmth 24 mos | −0.07 [−0.21, 0.07] | −0.02 [−0.16, 0.12] | 0.16** [0.05, 0.28] | 0.09 [−0.01, 0.18] | −0.14* [−0.26, −0.02] |
| 4. Interaction Effects | |||||
| Marijuana × Warmth 24 mos | −0.25 [−0.79, 0.30] | 0.05 [−0.53, 0.63] | −0.58** [−1.03, −0.13] | −0.10 [−0.48, 0.28] | 0.54* [0.06, 1.03] |
Note: Marijuana = Any marijuana use during pregnancy (yes/no). Bold values indicate statistically significant results. *p < 0.05. **p < 0.01.
3.3. Maternal Warmth as a Moderator of Prenatal Substance Use and Child Temperament (Hypothesis 2)
Results of the moderation analyses are presented in Tables 3, 4, 5, 6, 7, 8. Overall, moderation effects varied depending on the type of substance, the specific child outcome, the timing of substance use (overall pregnancy or 1st trimester‐only‐use), and the frequency of use (binary or continuous). For alcohol, no significant moderation effects were found (Tables 3, 4, 5, 6, 7, 8). Whether alcohol use was measured as overall, 1st use specific, or by frequency, maternal warmth at either 12‐ or 24‐months did not significantly interact with alcohol exposure in relation to any child temperament outcomes. In contrast, maternal warmth did moderate the association between tobacco exposure and certain child outcomes (Tables 3, 4, 5, 6, 7, 8; Figure 1A–C). For social fear, the association between frequency of tobacco use and child outcomes depended on maternal warmth at 24 months; the interaction was modest (β = −0.04, 95% CI [−0.08, 0.00]). Johnson–Neyman probing indicated that among dyads characterized by higher maternal warmth (+1 SD), the frequency of tobacco use was associated with lower child social fear (β = −0.05, 95% CI [−0.10, 0.00]; Figure 1A). No associations were observed at mean or lower levels of warmth. Because the moderation pattern for first‐trimester tobacco use (β = −0.05, 95% CI [−0.10, 0.00]) closely paralleled that observed for tobacco use frequency, with comparable regions of significance identified via Johnson–Neyman probing (β = −0.07, 95% CI [−0.13, −0.01]), those effects are presented in Supporting Information S1: Figure S1. Maternal warmth at 24 months moderated the association between prenatal tobacco use frequency and child pleasure (β = 0.02, 95% CI [0.00, 0.05]; Figure 1B). Simple slopes indicated higher tobacco use was associated with lower pleasure at low maternal warmth (−1 SD; β = −0.03, 95% CI [−0.04, −0.01]), but not at mean or high levels of warmth. A modest interaction emerged between tobacco use frequency and maternal warmth at 12 months in relation to child activity (β = 0.05, 95% CI [0.00, 0.09]). Probing this interaction using the Johnson–Neyman technique indicated at low levels of maternal warmth (−1 SD), greater frequency of prenatal tobacco use was associated with lower toddler activity levels (β = −0.04, 95% CI [−0.07, 0.00]; Figure 1C). Associations at mean and high levels of maternal warmth were not significant.
FIGURE 1.
Interaction of Prenatal Tobacco Use and Maternal Warmth on Child Regulation and Reactivity at 24 Months. Predicted values represent the composite score for child regulation and reactivity at 24 months, plotted at low (−1 SD), moderate (mean), and high (+1 SD) levels of maternal warmth (12 and 24 months) for low (−1 SD), moderate (Mean), and high (+1 SD) levels of prenatal tobacco use. All estimates are adjusted for maternal age, race, and child sex. The significant interaction between 1st trimester tobacco and social fear, consistent with the frequency model, is shown in Supporting Information S1: Figure S1.
Similarly, maternal warmth at 24 months moderated the association between prenatal marijuana exposure and some child outcomes (Tables 7 and 8; Figure 2A–B). The interaction between prenatal marijuana exposure and maternal warmth at 24 months was negatively significant (β = −0.58, 95% CI [−1.03, −0.13]) for child interest. Probing this interaction using simple slopes revealed that at high levels of maternal warmth at 24 months, prenatal marijuana exposure was associated with lower child interest (β = −0.50, 95% CI [−1.01, 0.01]; Figure 2A). For activity levels, the interaction between prenatal marijuana exposure and maternal warmth was significant (β = 0.54, 95% CI [0.06, 1.03]). At lower levels of maternal warmth (−1 SD), prenatal marijuana exposure was associated with lower child activity (β = −0.74, 95% CI [−1.37, −0.10]), whereas this association was not observed at higher levels of warmth (Figure 2B).
FIGURE 2.
Interaction of Prenatal Marijuana Use and Maternal Warmth on Child Regulation and Reactivity at 24 Months. Predicted values represent the composite score for child regulation and reactivity at 24 months, plotted at low (−1 SD), moderate (mean), and high (+1 SD) levels of maternal warmth (24 months) for prenatal marijuana use (Yes/No). All estimates are adjusted for maternal age, race, and child sex, which were held at their sample means.
3.4. Maternal Warmth as a Mediator Between Prenatal Substance Use and Child Temperament (Hypothesis 3)
Structural equation modeling results are presented in Tables 9, 10, 11, 12, 13, 14. Tests of model fit generally indicated acceptable fit for all estimated models (i.e., alcohol model for anger with maternal warmth at 24 months: χ 2(3) = 1.19, p = 0.53; RMSEA = 0; CFI = 1.00, SRMR = 0.02). A small number of models showed CFIs slightly below the conventional 0.90 cutoff (e.g., tobacco–interest model with maternal warmth at 24 months: χ 2(3) = 3.94, p = 0.27; RMSEA = 0.04; CFI = 0.86; SRMR = 0.03). These models were highly parsimonious with very small degrees of freedom (df = 3), a condition under which incremental fit indices such as the CFI can be unstable. Because absolute fit indices (χ 2, RMSEA, SRMR) consistently indicated good fit and CFIs closely approached recommended thresholds, all models were retained and interpreted as adequately fitting the data. Detailed fit indices for all models are reported in Supporting Information S1: Tables S2–S7. No specific indirect effects via maternal warmth reached statistical significance, indicating maternal warmth did not mediate the relationship between prenatal tobacco, alcohol, or marijuana exposure and any child outcomes. These results were also consistent for frequency and timing of use.
TABLE 9.
Mediation models examining prenatal alcohol use and child outcomes, with maternal warmth at 12 Months as a mediator.
|
Estimates |
Models by Outcome Variable Predicted | ||||
|---|---|---|---|---|---|
| Model 1: Anger | Model 2: Social fear | Model 3: Interest | Model 4: Pleasure | Model 5: Activity | |
| Alcohol | |||||
| Mother's age | −0.02 [−0.04, 0.01] | −0.02 [−0.05, 0.01] | 0.00 [−0.03, 0.02] | −0.02 [−0.04, 0.00] | −0.03* [−0.05, 0.00] |
| Child's sex | 0.18 [−0.10, 0.45] | −0.01 [−0.32, 0.30] | −0.04 [−0.28, 0.19] | 0.02 [−0.18, 0.22] | 0.03 [−0.23, 0.28] |
| Maternal race | 0.07 [−0.10, 0.28] | −0.08 [−0.26, 0.17] | 0.04 [−0.12, 0.19] | 0.08 [−0.06, 0.21] | −0.01 [−0.17, 0.17] |
| Prediction paths | |||||
| Alcohol → Outcome | 0.05 [−0.29, 0.38] | 0.34 [−0.13, 0.78] | −0.35* [−0.67, −0.01] | −0.06 [−0.33, 0.22] | −0.26 [−0.62, 0.10] |
| Alcohol → Warmth 12 mos | −0.30 [−0.73, 0.10] | −0.37 [−0.81, 0.04] | −0.30 [−0.73, 0.10] | −0.31 [−0.76, 0.12] | −0.36 [−0.79, −0.04] |
| Warmth 12 mos → Outcome | −0.02 [−0.20, 0.15] | 0.07 [−0.10, 0.26] | −0.09 [−0.21, 0.03] | 0.04 [−0.08, 0.17] | −0.04 [−0.21, 0.08] |
| Indirect paths | |||||
| Alcohol → Warmth 12 mos → Outcome | 0.01 [−0.05, 0.08] | −0.03 [−0.12, 0.05] | 0.03 [−0.01, 0.11] | −0.01 [−0.08, 0.03] | 0.02 [−0.04, 0.10] |
| 1st trimester alcohol | |||||
| Mother's age | −0.01 [−0.04, 0.01] | −0.02 [−0.05, 0.01] | −0.01 [−0.03, 0.02] | −0.02 [−0.04, 0.00] | −0.03** [−0.05, −0.01] |
| Child's sex | 0.18 [−0.08, 0.46] | 0.01 [−0.29, 0.32] | −0.07 [−0.30, 0.16] | 0.02 [−0.18, 0.21] | 0.01 [−0.24, 0.25] |
| Maternal race | 0.07 [−0.10, 0.28] | −0.10 [−0.28, 0.16] | 0.05 [−0.11, 0.21] | 0.08 [−0.06, 0.21] | 0.00 [−0.16, 0.18] |
| Prediction paths | |||||
| Alcohol → Outcome | −0.02 [−0.22, 0.17] | 0.03 [−0.04, 0.32] | −0.08 [−0.29, 0.01] | −0.02 [−0.22, 0.13] | −0.05 [−0.12, 0.18] |
| Alcohol → Warmth 12 mos | −0.12 [−0.38, 0.10] | −0.14 [−0.34, 0.06] | −0.11 [−0.37, 0.10] | −0.11 [−0.36, 0.11] | −0.14 [−0.34, 0.06] |
| Warmth 12 mos → Outcome | −0.03 [−0.19, 0.15] | 0.06 [−0.13, 0.24] | −0.08 [−0.20, 0.03] | 0.04 [−0.08, 0.17] | −0.03 [−0.19, 0.09] |
| Indirect paths | |||||
| Alcohol → Warmth 12 mos → Outcome | 0.00 [−0.03, 0.04] | −0.01 [−0.05, 0.02] | 0.01 [−0.01, 0.05] | 0.00 [−0.02, 0.00] | 0.00 [−0.02, 0.04] |
| Frequency of alcohol | |||||
| Mother's age | −0.01 [−0.04, 0.01] | −0.02 [−0.05, 0.01] | −0.01 [−0.03, 0.02] | −0.02 [−0.03, 0.00] | −0.03 [−0.05, −0.01] |
| Child's sex | 0.18 [−0.08, 0.45] | 0.01 [−0.29, 0.32] | −0.07 [−0.30, 0.16] | 0.02 [−0.18, 0.21] | 0.01* [−0.24, 0.25] |
| Maternal race | 0.07 [−0.10, 0.28] | −0.10 [−0.28, 0.16] | 0.05 [−0.10, 0.21] | 0.08 [−0.06, 0.21] | −0.01 [−0.17, 0.18] |
| Prediction paths | |||||
| Alcohol → Outcome | −0.02 [−0.12, 0.08] | 0.01 [−0.04, 0.10] | −0.02 [−0.10, 0.06] | −0.02 [−0.08, 0.07] | −0.06 [−0.13, 0.04] |
| Alcohol → Warmth 12 mos | −0.04 [−0.19, 0.08] | −0.08 [−0.18, 0.05] | −0.06 [−0.20, 0.04] | −0.06 [−0.16, 0.08] | −0.08 [−0.18, 0.05] |
| Warmth 12 mos → Outcome | −0.03 [−0.20, 0.14] | 0.05 [−0.13, 0.24] | −0.08 [−0.20, 0.04] | 0.04 [−0.08, 0.17] | −0.04 [−0.20, 0.09] |
| Indirect paths | |||||
| Alcohol → Warmth 12 mos → Outcome | 0.00 [−0.01, 0.02] | 0.00 [−0.03, 0.01] | 0.00 [−0.01, 0.02] | 0.00 [−0.02, 0.01] | 0.00 [−0.01, 0.02] |
Note: Alcohol = Any alcohol use during pregnancy (yes/no). 1st Trimester Alcohol = Alcohol consumed only in the first trimester. Frequency of Alcohol = Amount of alcohol consumed throughout the entire pregnancy. Bold values indicate statistically significant results. *p < 0.05. **p < 0.01.
TABLE 10.
Mediation models examining prenatal alcohol use and child outcomes, with maternal warmth at 24 Months as a mediator.
|
Estimates |
Models by outcome variable predicted | ||||
|---|---|---|---|---|---|
| Model 1: Anger | Model 2: Social fear | Model 3: Interest | Model 4: Pleasure | Model 5: Activity | |
| Alcohol | |||||
| Mother's age | −0.02 [−0.04, 0.01] | −0.03 [−0.05, 0.00] | 0.00 [−0.02, 0.02] | −0.01 [−0.02, 0.01] | −0.02* [−0.04, 0.00] |
| Child's sex | 0.18 [−0.10, 0.45] | 0.11 [−0.13, 0.35] | 0.06 [−0.12, 0.25] | −0.03 [−0.18, 0.12] | 0.05 [−0.15, 0.25] |
| Maternal race | 0.07 [−0.10, 0.28] | −0.06 [−0.23, 0.14] | 0.08 [−0.04, 0.21] | 0.08 [−0.02, 0.18] | 0.05 [−0.07, 0.19] |
| Prediction paths | |||||
| Alcohol → Outcome | 0.05 [−0.29, 0.38] | 0.04 [−0.30, 0.39] | −0.25 [−0.53, 0.04] | −0.09 [−0.29, 0.10] | −0.24 [−0.53, 0.06] |
| Alcohol → Warmth 24 mos | −0.30 [−0.73, 0.10] | 0.04 [−0.28, 0.32] | 0.10 [−0.14, 0.32] | 0.11 [−0.14, 0.34] | −0.01 [−0.34, 0.26] |
| Warmth 24 mos → Outcome | −0.02 [−0.20, 0.15] | 0.01 [−0.14, 0.16] | 0.12* [0.01, 0.25] | 0.07 [−0.01, 0.16] | −0.10 [−0.22, 0.02] |
| Indirect paths | |||||
| Alcohol → Warmth 24 mos → Outcome | 0.01 [−0.05, 0.08] | 0.00 [−0.02, 0.03] | 0.01 [−0.02, 0.04] | 0.01 [−0.01, 0.03] | 0.00 [−0.03, 0.05] |
| 1st trimester alcohol | |||||
| Mother's age | 0.00 [−0.02, 0.02] | −0.03* [−0.05, 0.00] | 0.00 [−0.02, 0.01] | −0.01 [−0.02, 0.01] | −0.02* [−0.04, 0.00] |
| Child's sex | 0.17 [−0.05, 0.39] | 0.10 [−0.13, 0.34] | 0.05 [−0.13, 0.24] | −0.03 [−0.18, 0.12] | 0.04 [−0.16, 0.24] |
| Maternal race | 0.12 [−0.02, 0.30] | −0.06 [−0.23, 0.14] | 0.08 [−0.03, 0.22] | 0.08 [−0.02, 0.18] | 0.06 [−0.06, 0.21] |
| Prediction paths | |||||
| Alcohol → Outcome | 0.01 [−0.12, 0.11] | −0.04 [−0.17, 0.08] | −0.02 [−0.15, 0.12] | 0.00 [−0.11, 0.10] | −0.06 [−0.12, 0.08] |
| Alcohol → Warmth 24 mos | −0.04 [−0.32, 0.15] | −0.07 [−0.24, 0.13] | 0.00 [−0.08, 0.14] | 0.00 [−0.08, 0.15] | −0.07 [−0.24, 0.12] |
| Warmth 24 mos → Outcome | −0.06 [−0.18, 0.04] | 0.00 [−0.14, 0.16] | 0.12 [0.00, 0.24] | 0.07 [−0.01, 0.16] | −0.10 [−0.23, 0.02] |
| Indirect paths | |||||
| Alcohol → Warmth 24 mos → Outcome | 0.00 [−0.01, 0.03] | 0.00 [−0.02, 0.02] | 0.00 [−0.01, 0.02] | 0.00 [−0.01, 0.02] | 0.01 [−0.02, 0.04] |
| Frequency of alcohol | |||||
| Mother's age | 0.00 [−0.02, 0.02] | −0.02* [−0.05, 0.00] | 0.00 [−0.02, 0.01] | −0.01 [−0.02, 0.01] | −0.02* [−0.04, 0.00] |
| Child's sex | 0.17 [−0.05, 0.39] | 0.10 [−0.13, 0.34] | 0.05 [−0.12, 0.24] | −0.03 [−0.18, 0.12] | 0.04 [−0.16, 0.24] |
| Maternal race | 0.12 [−0.02, 0.30] | −0.07 [−0.23, 0.14] | 0.08 [−0.02, 0.22] | 0.08 [−0.02, 0.18] | 0.06 [−0.07, 0.20] |
| Prediction paths | |||||
| Alcohol → Outcome | 0.00 [−0.08, 0.06] | −0.04 [−0.13, 0.02] | −0.01 [−0.08, 0.07] | −0.03 [−0.09, 0.05] | −0.06 [−0.12, 0.01] |
| Alcohol → Warmth 24 mos | 0.03 [−0.12, 0.12] | 0.00 [−0.12, 0.11] | 0.04 [−0.04, 0.12] | 0.04 [−0.04, 0.12] | −0.01 [−0.12, 0.10] |
| Warmth 24 mos → Outcome | −0.06 [−0.18, 0.04] | 0.01 [−0.14, 0.16] | 0.12 [0.00, 0.25] | 0.07 [−0.01, 0.16] | −0.10 [−0.22, 0.02] |
| Indirect paths | |||||
| Alcohol → Warmth 24 mos → Outcome | 0.00 [−0.01, 0.01] | 0.00 [−0.01, 0.01] | 0.00 [−0.01, 0.02] | 0.00 [0.00, 0.01] | 0.00 [−0.01, 0.02] |
Note: Alcohol = Any alcohol use during pregnancy (yes/no). 1st Trimester Alcohol = Alcohol consumed only in the first trimester. Frequency of Alcohol = Amount of alcohol consumed throughout the entire pregnancy. Bold values indicate statistically significant results. *p < 0.05. **p < 0.01.
TABLE 11.
Mediation models examining prenatal tobacco use and child outcomes, with maternal warmth at 12 Months as a mediator.
|
Estimates |
Models by outcome variable predicted | ||||
|---|---|---|---|---|---|
| Model 1: Anger | Model 2: Social fear | Model 3: Interest | Model 4: Pleasure | Model 5: Activity | |
| Tobacco | |||||
| Mother's age | −0.02 [−0.04, 0.01] | −0.03 [−0.05, 0.01] | 0.00 [−0.02, 0.02] | −0.01 [−0.03, 0.00] | −0.03** [−0.06, −0.01] |
| Child's sex | 0.19 [−0.08, 0.46] | 0.01 [−0.28, 0.31] | −0.08 [−0.29, 0.13] | 0.01 [−0.18, 0.20] | 0.04 [−0.19, 0.29] |
| Maternal race | 0.08 [−0.10, 0.29] | −0.11 [−0.30, 0.15] | 0.11 [−0.03, 0.28] | 0.10 [−0.02, 0.22] | −0.01 [−0.17, 0.18] |
| Prediction paths | |||||
| Tobacco → Outcome | −0.24 [−0.59, 0.11] | 0.06 [−0.29, 0.44] | −0.46** [−0.76, −0.16] | −0.18 [−0.40, 0.05] | −0.02 [−0.34, 0.31] |
| Tobacco → Warmth 12 mos | −0.07 [−0.38, 0.22] | −0.13 [−0.48, 0.18] | −0.14 [−0.44, 0.17] | −0.14 [−0.44, 0.16] | −0.13 [−0.44, 0.17] |
| Warmth 12 mos → Outcome | −0.06 [−0.23, 0.12] | 0.02 [−0.16, 0.20] | −0.08 [−0.19, −0.03] | 0.05 [−0.07, 0.18] | −0.04 [−0.20, 0.09] |
| Indirect paths | |||||
| Tobacco → Warmth 12 mos → Outcome | 0.00 [−0.03, 0.04] | 0.00 [−0.05, 0.03] | 0.01 [−0.02, 0.05] | −0.01 [−0.04, 0.02] | 0.00 [−0.02, 0.05] |
| 1st trimester tobacco | |||||
| Mother's age | −0.02 [−0.04, 0.01] | −0.03* [−0.06, 0.00] | 0.00 [−0.02, 0.02] | −0.01 [−0.03, 0.01] | −0.03** [−0.06, −0.01] |
| Child's sex | 0.18 [−0.08, 0.45] | 0.01 [−0.28, 0.32] | −0.10 [−0.31, 0.11] | 0.00 [−0.19, 0.19] | 0.04 [−0.20, 0.28] |
| Maternal race | 0.09 [−0.09, 0.31] | −0.15 [−0.33, 0.11] | 0.12 [−0.01, 0.27] | 0.12* [0.00, 0.24] | 0.00 [−0.17, 0.20] |
| Prediction paths | |||||
| Tobacco → Outcome | −0.04 [−0.09, 0.02] | 0.05* [0.00, 0.10] | −0.06 [−0.12, −0.02] | −0.04* [−0.07, 0.00] | −0.02 [−0.07, 0.04] |
| Tobacco → Warmth 12 mos | −0.01 [−0.06, 0.02] | −0.03 [−0.09, 0.01] | −0.02 [−0.08, 0.02] | −0.02 [−0.08, 0.02] | −0.02 [−0.08, 0.02] |
| Warmth 12 mos → Outcome | −0.06 [−0.23, 0.12] | 0.04 [−0.15, 0.21] | −0.08 [−0.20, 0.03] | 0.04 [−0.08, 0.17] | −0.04 [−0.20, 0.08] |
| Indirect paths | |||||
| Tobacco → Warmth 12 mos → Outcome | 0.00 [0.00, 0.01] | 0.00 [−0.01, 0.00] | 0.00 [0.00, 0.01] | 0.00 [−0.01, 0.00] | 0.00 [0.00, 0.01] |
| Frequency of tobacco | |||||
| Mother's age | −0.02 [−0.04, 0.01] | −0.03* [−0.06, 0.00] | 0.00 [−0.02, 0.02] | −0.01 [−0.03, 0.01] | −0.03 [−0.06, −0.01] |
| Child's sex | 0.17 [−0.09, 0.44] | 0.03 [−0.27, 0.33] | −0.13 [−0.34, 0.08] | −0.02 [−0.21, 0.17] | 0.04 [−0.20, 0.28] |
| Maternal race | 0.08 [−0.10, 0.29] | −0.13 [−0.32, 0.13] | 0.12 [−0.01, 0.26] | 0.12* [0.00, 0.24] | −0.01 [−0.17, 0.19] |
| Prediction paths | |||||
| Tobacco → Outcome | −0.02 [−0.06, 0.02] | 0.02 [−0.01, 0.06] | −0.04** [−0.06, 0.00] | −0.02 [−0.05, −0.01] | −0.01 [−0.04, 0.04] |
| Tobacco → Warmth 12 mos | 0.00 [−0.04, 0.03] | −0.01 [−0.05, 0.02] | −0.01 [−0.05, 0.02] | −0.01 [−0.05, 0.02] | −0.01 [−0.06, 0.02] |
| Warmth 12 mos → Outcome | −0.05 [−0.23, 0.12] | 0.03 [−0.16, 0.20] | −0.08 [−0.19, 0.03] | 0.04 [−0.08, 0.17] | −0.04 [−0.20, 0.08] |
| Indirect paths | |||||
| Tobacco → Warmth 12 mos → Outcome | 0.00 [0.00, 0.00] | 0.00 [0.00, 0.00] | 0.00 [0.00, 0.00] | 0.00 [0.00, 0.00] | 0.00 [0.00, 0.00] |
Note: Tobacco = Any tobacco use during pregnancy (yes/no). 1st Trimester Tobacco = Tobacco consumed only in the first trimester. Frequency of Tobacco = Amount of tobacco consumed throughout the entire pregnancy. Bold values indicate statistically significant results. *p < 0.05. **p < 0.01.
TABLE 12.
Mediation models examining prenatal tobacco use and child outcomes, with maternal warmth at 24 Months as a mediator.
|
Estimates |
Models by outcome variable predicted | ||||
|---|---|---|---|---|---|
| Model 1: Anger | Model 2: Social fear | Model 3: Interest | Model 4: Pleasure | Model 5: Activity | |
| Tobacco | |||||
| Mother's age | −0.01 [−0.03, 0.01] | −0.03* [−0.05, 0.00] | 0.00 [−0.02, 0.02] | −0.01 [−0.03, 0.00] | −0.02* [−0.04, 0.00] |
| Child's sex | 0.18 [−0.03, 0.40] | 0.10 [−0.13, 0.35] | 0.04 [−0.15, 0.21] | −0.03 [−0.18, 0.12] | 0.06 [−0.14, 0.25] |
| Maternal race | 0.12 [−0.02, 0.30] | −0.06 [−0.23, 0.15] | 0.10 [−0.01, 0.23] | 0.08 [−0.02, 0.19] | 0.05 [−0.08, 0.19] |
| Prediction paths | |||||
| Tobacco → Outcome | −0.10 [−0.37, 0.18] | −0.19 [−0.54, 0.16] | −0.13 [−0.43, 0.18] | 0.00 [−0.21, 0.20] | 0.00 [−0.26, 0.26] |
| Tobacco → Warmth 24 mos | −0.14 [−0.45, 0.14] | −0.15 [−0.50, 0.16] | −0.20 [−0.53, 0.08] | −0.16 [−0.47, 0.11] | −0.17 [−0.48, 0.10] |
| Warmth 24 mos → Outcome | −0.09 [−0.21, 0.02] | −0.02 [−0.18, 0.13] | 0.12* [0.01, 0.25] | 0.08 [0.00, 0.17] | −0.12* [−0.23, 0.01] |
| Indirect paths | |||||
| Tobacco → Warmth 24 mos → Outcome | 0.01 [−0.02, 0.05] | 0.00 [−0.02, 0.05] | −0.02 [−0.07, 0.01] | −0.01 [−0.06, 0.01] | 0.02 [−0.02, 0.06] |
| Mother's age | −0.01 [−0.03, 0.01] | −0.03 [−0.05, 0.00] | 0.00 [−0.02, 0.02] | −0.01 [−0.02, 0.01] | −0.02* [−0.04, 0.00] |
| 1st Trimester Tobacco | |||||
| Child's sex | 0.18 [−0.03, 0.40] | 0.10 [−0.13, 0.34] | 0.04 [−0.15, 0.21] | −0.03 [−0.18, 0.12] | 0.05 [−0.15, 0.24] |
| Maternal race | 0.13 [−0.01, 0.31] | −0.07 [−0.24, 0.14] | 0.10 [0.00, 0.22] | 0.09 [−0.01, 0.19] | 0.06 [−0.07, 0.20] |
| Prediction paths | |||||
| Tobacco → Outcome | −0.04 [−0.08, 0.00] | −0.02 [−0.08, 0.05] | −0.02 [−0.08, 0.04] | 0.00 [−0.04, 0.03] | −0.02 [−0.05, 0.02] |
| Tobacco → Warmth 24 mos | −0.01 [−0.07, 0.02] | −0.02 [−0.08, 0.02] | −0.03 [−0.09, 0.01] | −0.02 [−0.07, 0.02] | −0.02 [−0.08, 0.01] |
| Warmth 24 mos → Outcome | −0.10 [−0.21, 0.02] | −0.02 [−0.17, 0.14] | 0.12* [0.01, 0.25] | 0.08 [0.00, 0.17] | −0.12 [−0.24, 0.00] |
| Indirect paths | |||||
| Tobacco → Warmth 24 mos → Outcome | 0.00 [0.00, 0.01] | 0.00 [0.00, 0.01] | 0.00 [−0.01, 0.00] | 0.00 [−0.01, 0.00] | 0.00 [0.00, 0.01] |
| Frequency of tobacco | |||||
| Mother's age | −0.01 [−0.03, 0.01] | −0.03* [−0.05, 0.00] | 0.00 [−0.02, 0.02] | −0.01 [−0.02, 0.01] | −0.02* [−0.04, 0.00] |
| Child's sex | 0.17 [−0.04, 0.40] | 0.10 [−0.13, 0.34] | 0.02 [−0.17, 0.19] | −0.04 [−0.19, 0.11] | 0.05 [−0.15, 0.24] |
| Maternal race | 0.13 [−0.02, 0.30] | −0.07 [−0.24, 0.13] | 0.11 [0.01, 0.23] | 0.09 [−0.01, 0.19] | 0.06 [−0.08, 0.20] |
| Prediction paths | |||||
| Tobacco → Outcome | −0.02* [−0.04, 0.00] | −0.01 [−0.05, 0.02] | −0.02 [−0.04, 0.02] | −0.01 [−0.03, 0.01] | −0.01 [−0.03, 0.02] |
| Tobacco → Warmth 24 mos | −0.01 [−0.05, 0.01] | −0.01 [−0.06, 0.00] | −0.02 [−0.07, 0.00] | −0.01 [−0.05, 0.00] | −0.01 [−0.05, 0.00] |
| Warmth 24 mos → Outcome | −0.10 [−0.22, 0.01] | −0.02 [−0.18, 0.13] | 0.11 [0.00, 0.23] | 0.07 [−0.01, 0.16] | −0.12* [−0.24, 0.00] |
| Indirect paths | |||||
| Tobacco → Warmth 24 mos → Outcome | 0.00 [0.00, 0.00] | 0.00 [0.00, 0.00] | 0.00 [−0.01, 0.00] | 0.00 [0.00, 0.00] | 0.00 [0.00, 0.01] |
Note: Tobacco = Any tobacco use during pregnancy (yes/no). 1st Trimester Tobacco = Tobacco consumed only in the first trimester. Frequency of Tobacco = Amount of tobacco consumed throughout the entire pregnancy. Bold values indicate statistically significant results. *p < 0.05. **p < 0.01.
TABLE 13.
Mediation models examining prenatal marijuana use and child outcomes, with maternal warmth at 12 Months as a mediator.
|
Estimates |
Models by outcome variable predicted | ||||
|---|---|---|---|---|---|
| Model 1: Anger | Model 2: Social fear | Model 3: Interest | Model 4: Pleasure | Model 5: Activity | |
| Marijuana | |||||
| Mother's age | −0.02 [−0.04, 0.00] | −0.03 [−0.05, 0.01] | −0.01 [−0.03, 0.02] | −0.02 [−0.03, 0.00] | −0.03** [−0.06, ‐0.01] |
| Child's sex | 0.18 [−0.08, 0.46] | −0.02 [−0.27, 0.33] | −0.09 [−0.30, 0.13] | 0.01 [−0.19, 0.19] | 0.04 [−0.19, 0.29] |
| Maternal race | 0.06 [−0.10, 0.26] | −0.09 [−0.28, −0.15] | 0.08 [−0.07, 0.23] | 0.09 [−0.04, 0.22] | −0.01 [−0.18, 0.18] |
| Prediction paths | |||||
| Marijuana → Outcome | −0.12 [−0.80, 0.57] | −0.54 [−1.27, 0.24] | −0.39* [−0.73, 0.04] | −0.10 [−0.66, 0.40] | −0.02 [−0.58, 0.69] |
| Marijuana → Warmth 12 mos | −0.01[−0.39, 0.34] | −0.07 [−0.45, 0.31] | 0.00 [−0.37, 0.34] | 0.00 [−0.37, 0.35] | 0.00 [−0.35, 0.35] |
| Warmth 12 mos → Outcome | −0.05 [−0.23, 0.12] | 0.02 [−0.16, 0.20] | −0.06 [−0.18, 0.06] | 0.05 [−0.06, 0.19] | −0.04 [−0.19, 0.09] |
| Indirect paths | |||||
| Marijuana → Warmth 12 mos → Outcome | 0.00 [−0.04, 0.04] | 0.00 [−0.04, 0.04] | 0.00 [−0.04, 0.03] | 0.00 [−0.04, 0.03] | 0.00 [−0.03, 0.03] |
Note: Marijuana = Any marijuana use during pregnancy (yes/no). Reported model parameters are unstandardized coefficients. Bold values indicate statistically significant results. *p < 0.05. **p < 0.01.
TABLE 14.
Mediation models examining prenatal marijuana use and child outcomes, with maternal warmth at 24 Months as a mediator.
|
Estimates |
Models by outcome variable predicted | ||||
|---|---|---|---|---|---|
| Model 1: Anger | Model 2: Social fear | Model 3: Interest | Model 4: Pleasure | Model 5: Activity | |
| Marijuana | |||||
| Mother's age | −0.01 [−0.03, 0.01] | −0.03** [−0.05, 0.00] | 0.00 [−0.02, 0.01] | −0.01 [−0.03, 0.00] | −0.02** [−0.04, −0.01] |
| Child's sex | 0.18 [−0.03, 0.41] | 0.10 [−0.12, 0.35] | 0.04 [−0.15, 0.22] | −0.03 [−0.18, 0.12] | 0.06 [−0.14, 0.25] |
| Maternal race | 0.12 [−0.01, 0.29] | −0.06 [−0.23, 0.13] | 0.10 [−0.02, 0.22] | 0.09 [−0.02, 0.19] | 0.06 [−0.08, 0.20] |
| Prediction paths | |||||
| Marijuana → Outcome | −0.28 [−0.73, 0.18] | −0.31 [−0.92, 0.35] | −0.16 [−0.61, 0.32] | −0.04 [−0.42, 0.30] | −0.32 [−0.80, 0.18] |
| Marijuana → Warmth 24 mos | 0.12 [−0.37, 0.43] | 0.11 [−0.50, 0.48] | 0.08 [−0.48, 0.42] | 0.11 [−0.42, 0.44] | 0.14 [−0.36, 0.45] |
| Warmth 24 mos → Outcome | −0.09 [−0.20, −0.03] | −0.02 [−0.16, 0.14] | 0.12* [0.02, 0.26] | 0.08 [0.00, 0.17] | −0.11 [−0.23, 0.00] |
| Indirect paths | |||||
| Marijuana → Warmth 24 mos → Outcome | −0.01 [−0.06, 0.04] | 0.00 [−0.05, 0.04] | 0.01 [−0.04, 0.08] | 0.01 [−0.04, 0.05] | −0.02 [−0.08, 0.03] |
Note: Marijuana = Any marijuana use during pregnancy (yes/no). Reported model parameters are unstandardized coefficients. Bold values indicate statistically significant results. *p < 0.05. **p < 0.01.
In our sensitivity analyses, we repeated all primary models for each of the three substances, including additional covariates, such as maternal education, marital status, and residence type. Results are presented in Supporting Information S1: S8–S19. While the majority of findings remained consistent, particularly for the mediation and moderation models, we observed some fluctuations in the direct effects of tobacco use: certain associations (i.e., with anger) became significant, while others (i.e., with pleasure) lost significance, suggesting these additional sociodemographic factors may influence some, but not all, of these child outcomes.
4. Discussion
This study examined substance‐specific associations between prenatal exposure to alcohol, tobacco, and marijuana and child emotion regulation and reactivity at 24 months (about 2 years), with each substance evaluated in separate analytic models. We also explored maternal warmth at 12 and 24 months as a potential moderator and mediator of these substance‐specific associations. Several key findings emerged. First, prenatal alcohol use was associated with lower child interest but showed no other significant associations. Second, tobacco use during pregnancy was associated with lower levels of child interest and pleasure (across all models), as well as with child anger when assessed by frequency and 1st trimester use. Third, maternal warmth moderated some of these associations: higher warmth appeared to buffer the impact of prenatal tobacco and marijuana use on certain child outcomes. Fourth, maternal warmth did not serve as a mediator in any prenatal substance use model. These findings are discussed in more detail below.
We observed the following direct effects: prenatal alcohol use was associated with lower child interest at 24 months, while tobacco use was associated with reduced interest, pleasure, and anger. The only significant direct effects of marijuana use were on child interest, though the lack of direct effects on other child outcomes may reflect the small number of mothers in our sample who reported marijuana use during pregnancy. These findings align with prior research demonstrating links between prenatal alcohol (Alvik et al. 2011; Jirikowic et al. 2016; Lin et al. 2018; O'Connor 2001; Reid and Petrenko 2018; Schoeps et al. 2018), tobacco exposure (Eiden et al. 2020; Froggatt et al. 2020a; Law et al. 2023; Sutin et al. 2018), and neurocognitive impairments in children, including disruptions in the development of temperament (Andre et al. 2020; Chu et al. 2022; Ruisch et al. 2018; Terrell et al. 2019). In contrast to alcohol and tobacco, prenatal marijuana use was not broadly associated with child temperament across domains; however, an association emerged with lower toddler interest, a temperament dimension closely linked to early attentional engagement and neurocognitive functioning. This aligns with prior work linking prenatal marijuana use to attention problems and lower engagement in toddlerhood (El Marroun et al. 2011; Ostlund et al. 2021). Moreover, these findings expand previous work by Schuetze et al. (2019), who didn't find prenatal marijuana exposure to be associated with toddler autonomic regulation. Overall, these results support the differential impact of prenatal substance exposures on early child temperament, highlighting the individual effects of alcohol, tobacco, and marijuana.
We did not find a buffering effect of maternal warmth on the association between prenatal alcohol use and child temperament. We suspect alcohol exerts a distinct and more damaging influence on child regulation and reactivity, an effect that may not be mitigated even by high levels of maternal warmth. This is consistent with prior findings indicating alcohol is a teratogen posing irreversible and lifelong risks to the central nervous system. In fact, when compared to other substances such as tobacco and marijuana, alcohol carries a greater risk of neurodevelopmental harm (Deyssenroth et al. 2024). Therefore, maternal warmth alone may not be a sufficient buffer against the adverse effects of prenatal alcohol exposure on child regulation and reactivity. This is in line with a study by Schuetze et al. (2020) which found sensitive caregiving can only buffer children from externalizing challenges when prenatal risk, including prenatal alcohol use, is relatively low. However, under high prenatal substance use, even sensitive parenting may not fully counteract the elevated risk for developmental difficulties.
Interestingly, prenatal tobacco use presented a different pattern of moderation effects that were based on both the timing of exposure (overall pregnancy or 1st trimester use) and the frequency of use (binary indicator or continuous variable). Notably, maternal warmth at 24 months moderated the association between 1st trimester tobacco exposure and child social fear, such that at higher levels of maternal warmth, prenatal tobacco exposure was associated with lower levels of social fear (see Supporting Information S1: Figure S1). Additionally, at higher levels of maternal warmth at 24 months, the frequency of prenatal tobacco use was associated with higher levels of pleasure compared to those with lower maternal warmth (see Figure 1B). These results suggest warm caregiving during infancy can buffer temperamental risks linked to prenatal tobacco exposure by reducing fearfulness and enhancing pleasure, an important aspect of regulation. Our findings with toddlers build on prior work by Clark et al. (2019), which showed high maternal responsiveness can buffer the negative effects of prenatal tobacco exposure on effortful control in 5‐year‐olds. Both our study and Clark et al. (2019) find early parenting to be critical for buffering children from adverse prenatal environments, and our study demonstrates these effects at an age that is foundational for later neurodevelopmental outcomes. Additionally, our data suggest maternal warmth is particularly protective when prenatal tobacco exposure occurs during the first trimester, a known sensitive period for fetal neurodevelopment (Eiden et al. 2018).
In the context of prenatal marijuana exposure, maternal warmth at 24 months demonstrated a nuanced and somewhat counterintuitive pattern of associations with child outcomes. Specifically, in the moderation analysis, when maternal warmth was low, the association between prenatal marijuana exposure and child activity was negative. However, at high levels of maternal warmth, prenatal marijuana use was associated with lower levels of interest in children at 24 months compared to those who did not use marijuana. This pattern is somewhat counterintuitive, as greater maternal warmth is generally associated with increased child engagement and curiosity (Belsky et al. 1980; Warren and Brady 2007). One possible explanation for this counterintuitive finding lies in previous research suggesting prenatal marijuana exposure may alter early neurodevelopment in ways that impair the child's ability to benefit from environmental input, even when it is positive. Prior research suggests prenatal substance exposure can be associated with early regulatory profiles marked by reduced arousal, attentional engagement, and exploratory behavior, often described as hyporeactivity (Chasnoff 1985). This hyporeactivity may dampen observable engagement with the child's surroundings and attenuate expected relationships with warm caregiving. This finding may suggest a potential developmental pathway through which prenatal marijuana use is associated with later adjustment outcomes, including autism spectrum disorder and internalizing disorder (Corsi et al. 2020; Moore et al. 2023), through early hyporeactivity. As such, the present finding highlights a specific context in which these hyporeactive behaviors may emerge, and future studies should examine this relationship in relation to later child adjustment to better capture typologies of adjustment. Taken together, this work underscores the importance of considering how prenatal substance use may be associated with early neurodevelopmental vulnerabilities, such as hyporeactivity.
Additionally, we found the moderating effects of maternal warmth on child outcomes varied by the timing of parenting assessment. Specifically, maternal warmth at 24 months emerged as a significant moderator in several models, whereas maternal warmth at 12 months showed limited influence, only moderating activity levels in relation to the frequency of prenatal tobacco exposure. Although initially unexpected, this pattern is consistent with prior research suggesting parenting demands evolve substantially between the first and second year of life. For instance, Waters and colleagues (1991) note parenting at 12 months typically focuses on meeting basic physical and emotional needs, such as feeding, soothing, and protecting. In contrast, by 24 months, parenting increasingly involves the use of guidance, structure, and limit‐setting, behaviors that support more complex cognitive and emotional development. At this stage, parenting shifts from primarily providing positive engagement to scaffolding emerging skills such as self‐regulation, language, and prosocial behavior (Bernier et al. 2010; Landry et al. 2003; Pungello et al. 2009; Tamis‐LeMonda et al. 1996). The developmental advances occurring at 24 months may allow children to more fully perceive, interpret, and respond to caregiver behavior, potentially explaining why maternal warmth showed moderating effects on regulation outcomes at this time point (Ballarotto et al. 2023). Importantly, the broader pattern of our results suggests maternal warmth may become a more significant moderator as children's capacities for interpreting and responding to their caregivers mature. Even in models where moderation effects did not reach significance, we observed stronger trends toward moderation at 24 months than at 12 months. This consistency highlights the potential developmental sensitivity of toddlerhood for the buffering effects of parenting. It also raises the possibility that global assessments of parenting conducted too early may miss crucial interactions between caregiving and temperamental systems, especially in the context of prenatal substance exposure.
Interestingly, the only significant parental warmth moderation at 12 months highlights an important feature of parenting at 12 months. Specifically, we found that at low levels of maternal warmth at 12 months, frequency of prenatal tobacco use was associated with decreased activity at 24 months compared to high levels of maternal warmth. One explanation may be 12 months represents a sensitive period for emerging mobility and autonomy, during which maternal warmth (involvement and responsiveness) plays a crucial role in promoting exploration and activity (van Huisstede et al. 2019). When maternal warmth is lacking during this window, infants may receive less encouragement to move, fewer opportunities for gross motor play, or may model more sedentary behavior, which could further compound the neurodevelopmental impact of prenatal tobacco exposure (Mesquita et al. 2020).
In contrast to our hypotheses and prior findings in the literature, our results do not support the role of maternal warmth (at either 12‐ or 24‐months) as a mediator of the association between prenatal substance exposure and child regulation and reactivity. Specifically, none of the mediation analyses reached significance. This finding contrasts with previous research suggesting parenting behaviors, particularly negative parenting, frequently mediate the effects of prenatal substance exposure on child developmental outcomes (Peisch et al. 2018). For example, studies have shown substance use during pregnancy is associated with increased risks of negative postnatal parenting (Guyon‐Harris et al. 2023; Jacques et al. 2020; Mayes and Truman 2002), and these parenting behaviors can serve as key mechanisms through which prenatal exposure negatively affects children. In contrast, our findings indicate that, although we observed some direct negative effects of prenatal alcohol and tobacco exposure, particularly on child interest and pleasure, these effects did not operate through lower maternal warmth. In addition, there was no association between prenatal substance use and maternal warmth, suggesting prenatal substance exposure does not necessarily diminish positive parenting behaviors. Parents may still engage in warm, responsive interactions, but it may co‐occur with an increased use of negative parenting behaviors (i.e., Schuetze et al. 2019). The absence of strong positive parenting does not automatically imply the presence of harsh or intrusive behavior; rather, lower warmth may reflect more withdrawn or disengaged parenting. This highlights the importance of examining the full spectrum of parenting behaviors, as different types of parenting (both positive and negative) may operate through distinct mechanisms to influence child outcomes. These results support resilience theory and environmental sensitivity, such that a protective factor, such as maternal warmth, can buffer against biological vulnerabilities reducing its impact on later outcomes (Hartman et al. 2023; Zimmerman 2013). This might be due to the additional demands for autonomy and control that the toddler demands at 24 months and is better picked up when assessing regulation and reactivity. Specifically, parental warmth at 24 months might be serving as a model for the child, teaching the child how to better respond to their environment (Kiss et al. 2014; Kopp 1982).
These findings have important implications for how we understand and address prenatal substance use, particularly in the context of when and how much exposure occurs. In our sample, many women who reported tobacco or alcohol use during pregnancy did so primarily in the first trimester, probably before recognizing they were pregnant. For example, reports of first‐trimester tobacco use include women who later quit, and the frequency of use varied widely, from occasional use to daily smoking. These nuances in the timing and frequency of exposure are critical, as early gestational periods are especially sensitive for fetal neurodevelopment. While encouraging early pregnancy awareness can be helpful from a public health perspective, it is important to recognize not all pregnancies are planned or detected early, especially within the first few weeks when much of this exposure may occur. Many individuals may not realize they are pregnant until well into the first trimester, and access to early testing or care is not always equitable. Acknowledging this complexity is essential to avoid blaming individuals and instead emphasizes the need for broader structural supports and public health strategies that prioritize education, access to reproductive health services, and nonjudgmental prenatal care.
These insights have important implications for early parenting interventions and prevention efforts. Rather than focusing only on mothers who use substances during pregnancy, our findings highlight the broader value of universal parenting support during the early years of a child's life. Regardless of prenatal exposures, warm and responsive caregiving can promote healthier child temperament and help buffer against early life stress. However, access to evidence‐based parenting interventions remains limited. A review by Jeong et al. (2021) found that of 102 early childhood parenting trials conducted globally, only 40 took place in the United States, presenting a significant gap in the country. Expanding access to supportive, affordable parenting interventions can help foster stronger parent‐child relationships and improve developmental outcomes for families broadly, without relying on assumptions about pregnancy recognition or singling out specific populations.
As with all research, this study has limitations. Our first limitation is the measurement of prenatal substance use, which relied on mothers' self‐reported responses. Given the sensitivity and social stigma surrounding substance use during pregnancy, there may have been a tendency for participants to answer in socially desirable ways. This issue may have been particularly pronounced for marijuana use, as the sample was collected between 1998 and 2002, a time when marijuana was illegal across the United States. This legal context likely increased participants' reluctance to disclose usage, reducing power. This social desirability may have been heightened by the demographic composition of the sample, which included a racially and ethnically diverse population who might be reluctant to disclose stigmatizing experiences, such as prenatal substance use (Salameh et al. 2019; Treder et al. 2022). Second, although the overall sample size was adequate (n = 404), the number of participants reporting using at least one prenatal substance use (n = 115), particularly marijuana and alcohol use (n = 20), was relatively small. This limited prevalence reduces statistical power to detect smaller effects (especially for trimester‐specific exposure) and might result in less stable estimates. It also limits the generalizability of the findings to populations with higher levels of prenatal substance use. As a result, the observed associations should be interpreted cautiously and should be replicated in larger and higher risk samples. Third, although we accounted for several demographic and contextual covariates, the possibility of residual confounding remains. Unmeasured factors, such as maternal mental health, stress levels, or postnatal substance use, may influence caregiving behaviors and the postnatal environment. While prior longitudinal research suggests prenatal substance exposure may exert effects independent of postnatal use (Dodge et al. 2019; Håberg et al. 2010; Knopik 2009), future studies should incorporate assessments of postnatal substance use and maternal psychosocial functioning to more clearly disentangle prenatal programming effects from ongoing environmental influences. Finally, it is likely maternal warmth and child temperament influences one another over time in a bidirectional manner (Wang and Gai 2024). However, the present study focused solely on whether maternal warmth functioned as a mediator or moderator in the relationship between prenatal substance use and child regulation and reactivity, without examining these potential reciprocal effects.
In sum, this study shows prenatal substance use is associated with child temperament (an important aspect of neurodevelopment related to executive functioning), while maternal warmth can offer protection, although its buffering effect varies depending on the context. Based on our results, it is suggested that while maternal warmth can moderate some of the adverse effects of prenatal substance use, its protective capacity depends on multiple factors: the type of substance, timing and frequency of exposure, child outcome assessed (regulation vs. reactivity), and when maternal warmth is observed. Given these results, early identification of prenatal substance use is essential, along with providing mothers timely and comprehensive support. Interventions should address not only the risk factors associated with prenatal substance use but also promote the development of sensitive and responsive caregiving. By supporting maternal well‐being and parenting skills early in a child's life, particularly within the first 2 years, we may enhance developmental outcomes for children and reduce the intergenerational impact of prenatal adversity.
Author Contributions
Maria Balaceanu: conceptualization, writing – review and editing, writing – original draft, methodology, visualization, formal analysis, software. Stephanie M. Engel: investigation, methodology, visualization, writing – review and editing. Amanda M. Ramos: conceptualization, methodology, visualization, supervision, writing – review and editing.
Ethics Statement
The Mount Sinai Children's Environmental Health study was approved by the Institutional Review Board of the Mount Sinai School of Medicine. Informed consent was obtained from all participants prior to participation. This analysis was approved by the Utah State University Institutional Review Board #15286.
Conflicts of Interest
The authors declare no conflicts of interest.
Supporting information
Supporting Information S1
Acknowledgments
This research was supported by grant P01ES09584 (Wolff) from the National Institute of Environmental Health Sciences (NIEHS) and the Environmental Protection Agency (EPA). The funding agencies had no role in the study design, data analysis, interpretation of the results, or the writing of this report.
Balaceanu, Maria , Engel Stephanie M., and Ramos Amanda M.. 2026. “The Effect of Prenatal Substance Use and Maternal Parenting on Infant Reactivity and Regulation,” Infancy: e70107. 10.1111/infa.70107.
Handling Editor: Dorcas Magai
Data Availability Statement
The data that support these analyses may be available upon request from Dr. Engel with approval from IRB. The data are not publicly available due to ethical restrictions.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Supporting Information S1
Data Availability Statement
The data that support these analyses may be available upon request from Dr. Engel with approval from IRB. The data are not publicly available due to ethical restrictions.