Skip to main content
Environmental Epigenetics logoLink to Environmental Epigenetics
. 2025 Aug 8;11(1):dvaf024. doi: 10.1093/eep/dvaf024

Association between maternal perceived stress during pregnancy and offspring DNA methylation changes in HPA axis genes at birth in the ECHO Consortium

Krystin Jones 1, Bianca P Acevedo 2, Lyndsay A Avalos 3, Brennan H Baker 4,5, Nicole R Bush 6, Claudia Buss 7,8,9,10, Luke P Grosvenor 11, Alison E Hipwell 12, Kristine Marceau 13, Cindy T McEvoy 14, Wei Perng 15, Alexandra D W Sullivan 16, Irene Tung 17, Yeyi Zhu 18, Christine Ladd-Acosta 19,20,✉,2
PMCID: PMC12462613  PMID: 41020071

Abstract

Evidence has linked maternal exposure to stress during pregnancy with poor offspring health and neurodevelopmental outcomes. However, the precise mechanism by which this may occur has not been fully elucidated. In this study, we examined whether maternal perceived stress during pregnancy was associated with newborn blood DNA methylation (DNAm) in hypothalamic–pituitary–adrenal axis-related genes (NR3C1, FKBP5, and HSD11B2) in single CpG site and gene-based analyses. We analysed a subset of 661 mother–child pairs from the Environmental Influences on Child Health Outcomes cohort study that met our analytic inclusion criteria. Maternal perceived stress was measured during pregnancy using the perceived stress scale, and newborn DNAm was measured using the Illumina 450K and EPIC Beadchips in cord blood and dried blood spots. Single-site associations were evaluated using linear regression models, and gene-based associations were evaluated using mean burden and variance component tests, adjusted for sociodemographic and lifestyle covariates. Sex-stratified models were used to evaluate sex differential effects. Prenatal perceived stress was statistically significantly associated with newborn DNAm in one CpG site (cg06613263) in NR3C1 and with aggregate DNAm in NR3C1 and FKBP5. Aggregate DNAm in FKBP5 was more strongly associated with prenatal perceived stress in female infants. These results may have important implications for improving offspring health and well-being by providing molecular targets that can be used to identify high-risk individuals and as a basis for developing and evaluating effective behaviour and pharmaceutical interventions.

Keywords: perceived stress, pregnancy, DNA methylation, HPA axis

Introduction

Exposure to prenatal stress is a concerning public health problem among women in the USA. Data from the Pregnancy Risk Assessment Monitoring System shows that 70% of women reported experiencing at least one stressful life event (SLE) in the year prior to their infant’s birth, and prior studies have reported high rates of psychosocial stress among pregnant women in the USA [1–3]. Maternal stress exposure during pregnancy has been linked to various offspring health outcomes, including preterm birth, low birthweight, sleep disorders, and neurodevelopmental disorders [4–8]. However, the underlying biological mechanisms by which these associations may occur are not fully characterized [9, 10]. Understanding these mechanisms may provide a means of identifying at-risk individuals or to facilitate the development and evaluation of interventions that mitigate the potential harms of maternal stress exposure during pregnancy.

Foetal DNA methylation (DNAm) may be an important biological mechanism in the link between prenatal stress and offspring health and development. The epigenome acts as an interface between genes and the environment, and DNAm is among the most extensively studied forms of epigenetic modification [7, 11–14]. DNAm involves the reversible addition or removal of a methyl group to the cytosine nucleotides in the CpG sites of a gene, leading to increases or decreases in gene expression. The gestational period is one of large-scale, dynamic DNAm change, and this developmental window is marked by a heightened sensitivity to environmental stimuli, leading to changes in DNAm state [11]. In a process known as foetal programming, these DNAm changes lead to functional and organizational changes in various biological systems, including the central nervous, autonomic nervous, neuro-endocrine, and immune systems [7, 11]. Foetal programming may prime the individual for future environmental insults and also may lead to an increased susceptibility to adverse health outcomes across a range of life stages such as preterm birth, neuropsychiatric disorders in childhood, and chronic diseases in adulthood [7, 11, 15]. Indeed, DNAm changes have been associated with preterm birth and neurodevelopmental conditions [16–18]. It is important to consider these factors in analyses, as we do here, that examine prenatal perceived stress exposure associations with DNAm patterns in offspring.

The foetal hypothalamic–pituitary–adrenal (HPA) axis is likely an important target of these processes. The HPA axis plays a critical role in stress response and glucocorticoid regulation, and the foetal HPA axis has shown marked sensitivity to the intrauterine environment [7, 10, 11]. Maternal prenatal experiences of stress marked by persistently elevated maternal glucocorticoid levels create dysregulation of the foetal HPA axis, including greater offspring cortisol response to an environmental stressor and changes in basal cortisol levels, through a variety of processes, including DNAm changes in HPA axis-associated genes in the foetus [9, 10, 19, 20]. HPA dysregulation has in turn been linked to neuropsychiatric outcomes, including attention deficit hyperactivity disorder and depression in children and adolescents [21, 22].

A growing number of studies have examined associations between maternal stress during pregnancy and newborn DNAm in HPA axis-associated genes, using both single CpG site and gene-based methylation analyses [7, 23]. These studies have almost exclusively examined, and have largely found significant associations between, the Nuclear Receptor Subfamily 3 Group C Member 1 (NR3C1) gene, which is critical to HPA functioning by controlling the amount of cortisol in the body, and maternal stress during pregnancy [7, 23–28]. Comparatively, only a few studies have examined other relevant genes implicated in foetal HPA axis functioning and overall stress reactivity, including hydroxysteroid 11-beta dehydrogenase 2 (HSD11B2), which converts cortisol to inactive cortisone [29], and FK506-binding protein 5 (FKBP5), which modulates glucocorticoid receptor activity in response to stress [30]. Additionally, these studies have reported largely inconsistent results likely due to several factors, including small study sizes, choice of covariates, and choice of prenatal stress measure [31–34].

Much of this prior research has been conducted in small study populations with little racial, ethnic, or socioeconomic diversity. Many of these studies examined fewer than 200 parent–child pairs, and the largest to date examined 482 dyads. This introduces issues related to power and the generalizability of study results [27, 31]. Much of this prior work has also focused on self-report measures of objective stressors, and related psychopathology, such as maternal depression and anxiety, rather than measures of perceived stress or distress [24–26, 33, 35]. Perceived stress, however, may be a more useful measure of maternal stress than SLEs in these investigations. In proposed models of the stress process, perceived stress is considered more proximal to the body’s peripheral stress response and so may be more predictive of illness outcomes than SLEs [36, 37]. This is because the pathogenic effects of stressful events likely stem from the emotional, subjective response to the event, rather than from the event itself [38]. Furthermore, the same event can lead to differences in perceived stress between individuals with different personal or social contexts, including social support, family structure, and cultural values and norms, and as such measures of objective stress may imperfectly capture the stress response and its impact on foetal development [38].

Additionally, as stated previously, most such studies have prioritized DNAm in NR3C1 genes, limiting our understanding of the effect of prenatal maternal stress on DNAm across various HPA axis-relevant genes. Sex-specific effects are also largely understudied in these investigations, despite evidence of sex differences in foetal development and offspring susceptibility to adverse outcomes due to prenatal maternal stress exposure [7, 23]. Finally, studies that have examined the association between maternal stress during pregnancy and offspring gene-level DNAm have primarily used burden tests that use mean or median methylation levels to capture aggregate DNAm across the region of interest [31]. These methods facilitate gains in power by removing the need to correct for multiple testing as in single-site analyses. Additionally, as individual CpG sites are unlikely to act alone in regulating gene expression, aggregate methods may identify more functionally relevant changes in DNAm than single CpG analysis. However, these methods may fail to account for different directions and magnitude of effect among CpG sites, thus resulting in loss of power and a potential masking of associations [39].

In the current study, we aim to address these limitations using a large, racially and ethnically diverse, US population-based cohort by examining the association between maternal stress during pregnancy and neonatal blood DNAm in the HPA axis-associated genes, NR3C1, HSD11B2, and FKBP5, as well as sex-specific effects through both site and gene-based analyses using flexible and computationally efficient variance component tests like the sequence kernel association test (SKAT) primarily used in rare genetic variant analyses to facilitate gains in power [39–41]. Unlike the aggregate methods described previously, SKAT models methylation at CpG sites more flexibly across a gene, allowing different directions and magnitudes of effect at each site in a gene. This flexibility is advantageous when examining gene-level DNAm changes associated with an exposure of interest because methylation levels influence downstream gene expression differently depending on its location in a gene. For example, methylation at CpGs located in a gene promoter region typically decreases gene expression, and methylation at CpGs in the gene body typically increases gene expression. Therefore, by facilitating different direction and magnitudes of effect between sites, SKAT overcomes assumptions of simpler aggregate methylation tests that each CpG methylation site in a gene contributes equally to an outcome and in the same direction, which does not align with biologic expectations. In these analyses, we use data from the Environmental Influences on Child Health Outcomes (ECHO) Program and focus on prenatal perceived stress as a measure of psychological distress to capture the subjective, cognitive appraisal of life stress. We hypothesize that higher levels of maternal perceived stress during pregnancy will be associated with increases in newborn blood DNAm levels in NR3C1, HSD11B2, and FKBP5 genes and that effects will differ by child’s sex.

Methods

Overall study design

The ECHO Program is a multisite cohort study comprised of pregnancy and pediatric sites designed to understand how environmental factors from preconception to early childhood influence child health and development, with the goal of minimizing disease risk and promoting positive health and well-being [42]. The ECHO Program includes a diverse cohort of participants from all US states, the District of Columbia, Puerto Rico, and Native American Tribal Nations (see Knapp et al. [42] for more details) [43, 44].

Participants

To examine the association between prenatal perceived stress and newborn blood DNAm, we included a subset of ECHO participants in our analyses that met the following inclusion criteria: (1) the mother reported on perceived stress during pregnancy, (2) the pregnancy was a singleton gestation, and (3) the child had a high-quality (passed quality control; QC) blood-derived (umbilical cord blood or blood spot) DNAm measure on either the Illumina Infinium HumanMethylation450 or Infinium MethylationEPIC BeadChips. The final analytic sample consisted of 661 mother–child dyads (Supplementary Fig. 1) from four ECHO sites: Healthy Start, Autism Spectrum Disorder Enriched Risk Cohort (ASDER), Atlanta ECHO Cohort of Emory, and Madres. Site-specific recruitment methods and population characteristics are outlined in Supplementary Table 1.

Perceived stress during pregnancy

Prenatal Perceived stress was measured using the perceived stress scale (PSS) [45]. The PSS is the most widely used measure of perceived stress in epidemiologic research and captures the degree to which events in one’s life are considered stressful [38]. Two versions of the PSS were administered at ECHO sites included in these analyses: 10-item (PSS-10) and 14-item (PSS-14). Across scales, each item is scored on a 5-point Likert scale that ranges from never (0) to very often (4). Item response theory (IRT) was used to harmonize all available PSS data across participants to the perceived stress NIH toolbox T-score metric, which has a mean of 50 and a standard deviation of 10 in the general US population [46].

Some participants had multiple perceived stress T-score measurements during pregnancy, and prenatal perceived stress was measured between 8 and 38 weeks. As repeated measures were correlated in our sample (Pearson’s ⍴ = 0.63, P-value < .001), we generated a mean T score from all available time points to examine the effect of maternal perceived stress across the entire prenatal period. We treated perceived stress as both a continuous and a binary variable to evaluate the robustness of our findings. For binary perceived stress scores, population norms derived from a representative US sample were used to delineate T-score categories (low to medium (binary category 0): <60 and high (binary category 1): ≥60) [47].

DNAm measures

Sites used approved site-specific protocols to collect umbilical cord blood or newborn blood spots. DNAm was measured using the Illumina Infinium HumanMethylation450 or Infinium MethylationEPIC BeadChips. Raw participant data obtained from each site were run through the ECHO Illumina QC pipeline using the ‘minfi’ R/Bioconductor package, and β values (ranging from 0 for completely unmethylated to 1 for completely methylated) calculated for each probe and sample. Samples were filtered for locus-level technical failures, sex discrepancy, poor bisulfite conversion, high detection P-values (>1% probes with detP > .05), and low-quality probes (>1% probes beadC < 3). Similarly, probes for which >1% samples with detP > .05 and >1% of samples with beadC < 3, as well as those that were cross reactive or had a single nucleotide polymorphism (SNP) at the CpG site were removed. This processing was followed by normalization procedures using the normal-exponential out-of-band correction method. Cell type proportions were estimated using biospecimen type appropriate reference panels [48]. A total of 661 samples (524 on the 450K array and 137 on the EPIC array) that met study inclusion criteria passed QC across four study sites (Supplementary Fig. 1). From the 430 739 probes on the 450K BeadChip and 733 758 on the EPIC BeadChip that passed QC, we derived a set of 71 CpG sites found on both arrays located in the NR3C1, FKBP5, and HSD11B2 genes based on Illumina’s annotation files for the 450K and EPIC BeadChips that assign each CpG site to a UCSC known gene. Separately, we derived a second dataset of 66 CpG sites that passed QC annotated to the NR3C1, FKBP5, and HSD11B2 genes located on the EPIC array only to use in complementary analyses.

Covariates and effect modifiers

Covariates included maternal age at time of delivery, maternal education as an indicator for socioeconomic status, maternal prenatal depressive symptoms, prenatal alcohol consumption, maternal prenatal tobacco use, child’s sex, and cell type proportions. Maternal prenatal depressive symptoms, prenatal alcohol consumption, and maternal prenatal tobacco use may be mediators of the association between prenatal perceived stress and newborn DNAm. We add these factors as covariates in our models to examine the direct effect of perceived stress independent of these factors. We also analysed child’s sex as an effect measure modifier to evaluate sex-specific effects and examined the effects of preterm birth on results in sensitivity analyses. Notably, we do not adjust for ancestry principal components in our analyses as rather than conduct an epigenome-wide screen, we focus our analyses on three genes. As a result, there is less of a concern of confounding due to population stratification. Additionally, we do not adjust for self-reported race/ethnicity, as we do not expect these socially defined factors to confound the association between perceived stress during pregnancy and newborn blood DNAm.

Covariate information was obtained from demographic forms, registration data, medical record abstraction, lifestyle forms, and validated scales. Prenatal maternal depressive symptom scores were measured using the PROMIS v1.0—Depression 8a scored on the PROMIST-score metric (mean = 50, standard deviation = 10) [49]. Scores from other depression scales, including the Edinburgh postnatal depression scale, were converted to the PROMIST-score metric using crosswalk tables to facilitate the merging of data across studies as described previously [50]. Maternal alcohol consumption and tobacco use during pregnancy were assessed by self-report through ECHO lifestyle forms. Cell type proportions were estimated as described above. Finally, preterm birth was delineated as birth at ≥37 weeks’ gestation (binary category = 0) and birth at <37 weeks’ gestation (binary category = 1).

Statistical analysis

We conducted our analyses in R version 4.2.2 [51]. We calculated descriptive statistics of mother and child characteristics for the analytic sample using means (±SD) and proportions (%) where appropriate, overall and stratified by low-medium vs. high prenatal perceived stress. We imputed missing covariate data using random forest (‘missForest’ package in R) [52].

DNAm β-values (which represent the proportion of methylated sites in bulk tissues; 0 < β < 1) were log2 transformed to M-values for use in primary statistical analyses. We also conducted complementary analyses using DNAm β-values to estimate % change in DNAm to aid in interpretation.

Analyses were conducted in participants with 450K and EPIC BeadChip measures, separately and then meta-analysed. We used the comBat() function from the ‘sva’ R/Bioconductor package [53] to correct for known batch effects. Using the lmFit() function from the ‘limma’ R/Bioconductor package [54], we then used multivariate linear regression models to analyse the association between prenatal perceived stress treated as both a continuous and binary variable, and DNAm measures at each CpG site under study (71 overlapping sites and 66 EPIC array only sites), adjusting for maternal age at time of child’s birth, maternal depressive symptoms, maternal prenatal alcohol consumption, maternal prenatal tobacco use, maternal education, and child’s sex. We combined group-specific results through a fixed effects inverse variance weighted meta-analysis using the METAL software [55]. To investigate sex-specific effects, we also conducted our analyses in female-only and male-only samples and assessed statistical interaction between prenatal perceived stress and child sex. To account for multiple testing, we used a Bonferroni-corrected significance threshold of 0.05/number of sites.

Sensitivity analysis

We carried out sensitivity analyses to evaluate the impact of several factors on the results. To examine the effect of preterm birth, we re-ran analyses restricting to children born ≥37 weeks’ gestation as infants born preterm may have different DNAm profiles than infants carried to term [16, 17]. Additionally, we re-ran analyses to exclude ASDER, an autism spectrum disorder familial enriched site, to evaluate whether results were impacted by familial ASD risk. Finally, given the expected correlation between perceived stress during pregnancy and maternal depressive symptoms, we used Pearson correlation to evaluate the bivariate correlation between PSS and maternal prenatal depression and conducted sensitivity analyses in which we excluded maternal depressive symptoms from our models.

Gene-based tests

We conducted gene-based tests of the association between continuous prenatal perceived stress and neonatal blood DNAm in four regions using CpG sites shared between arrays and EPIC only CpG sites: (1) NR3C1 gene region, (2) FKBP5 gene region, (3) HSD11B2 gene region, and (4) all three genes together. Genes were delineated using Illumina’s annotation file for the 450K and EPIC BeadChips. Analyses were conducted in the full, female-only and male-only samples.

Mean DNAm level tests. Mean methylation levels were calculated across CpG sites in each of the four gene regions. We employed generalized linear regression models to regress mean methylation levels in each region onto prenatal perceived stress, adjusting for covariates.

SKAT. We used the SKA T function in the ‘SKAT’ R package to test for the cumulative effect of methylation across multiple sites simultaneously using the SKAT method [39]. SKAT is a computationally efficient variance component score test that evaluates the effect of multiple variants in a region on a phenotype [39]. Though traditionally used in rare variant associations studies, prior work has adopted the method for use in gene-based methylation tests due to improved power and accommodation of different directions of effect [40, 41]. We used four sets of SKAT parameters:

  1. (Primary) Linear kernel with equal weights (each site assigned a weight of 1).

  2. Quadratic kernel with equal weights (each site assigned a weight of 1).

  3. Linear kernel with sites weighted based on the effect estimate obtained in individual site analyses (1 + abs (effect estimate)).

  4. Quadratic kernel with sites weighted based on effect size obtained in individual site analyses (1 + abs (effect estimate)).

In secondary analyses, we reran SKAT using the SKAT-O or optimal test method to identify the optimal linear combination between SKAT and mean burden tests [56].

As above, we conducted analyses in participants with 450K and EPIC array measures separately, and the resulting effect estimates and P-values combined by meta-analysis. For gene-based tests, we used a significance threshold of P < .05.

Results

Analytic sample descriptive characteristics

A total of 661 mother–child dyads from four ECHO cohort sites met our inclusion criteria (Supplementary Table 1). In our analytic sample, ~10% of mothers reported high perceived stress levels (T-score ≥ 60) (Table 1). This proportion ranged from 3.6% at the MADRES cohort site to 12.5% at the ASDER cohort site (Supplementary Table 2). These mothers were less likely to identify as White (68% vs. 75%), less likely to identify as Hispanic (28% vs. 36%), more likely to report alcohol consumption (20% vs. 17%) and tobacco use (15.4% vs. 6.5%) during pregnancy, and they also had higher depressive symptom scores (mean = 54.48, SD = 5.52 vs. 46.20, SD = 7.58) than women who reported low or medium levels of prenatal perceived stress.

Table 1.

Descriptive characteristics of parent and child samples.

Prenatal perceived stress a
Covariate Total (N = 661) Low to medium perceived stress (N = 596) High perceived stress (N = 65) P-value
Maternal self-reported race %
 Black 110 (16.6) 97 (16.3) 13 (20.0) .098
 White 492 (74.4) 448 (75.2) 44 (67.7)  
 Other 59 (8.9) 51 (8.6) 9 (13.8)  
 Missing 2 (0.3)      
Self-reported Hispanic ethnicity (%)
 Hispanic 233 (35.2) 215 (36.1) 18 (27.7) .228
 Missing 1 (0.2)      
Maternal age at delivery
 Mean (SD) 28.10 (6.01) 28.26 (6.07) 26.57 .034
 Missing 0   (5.32)  
Gestational weeks at delivery
 Mean (SD) 38.97 (1.36) 38.98 (1.38) 38.88 .152
 Missing 0   (1.17)  
 Preterm birth (%) 29 (4.4) 28 (4.7) <5 (<5) .389
 Missing 0      
Child sex (%)        
 Female 325 (49.2) 295 (49.5) 30 (46.2) .703
 Missing 0      
Maternal depressive symptoms during pregnancy
 Mean (SD) 47.02 (7.80) 46.20 (7.58) 54.48 <.001
 Missing 15 (2.3)   (5.52)  
Prenatal alcohol consumption (%)
 Yes 113 (17.1) 100 (16.8) 13 (20.0) .630
 Missing 41 (6.2)      
Prenatal tobacco use (%)
 Yes 49 (7.4) 36 (6.5) 10 (15.4) .020
 Missing 0      
Maternal education (%)
 Less than high school 117 (17.7) 104 (17.4) 13 (20.0) .877
 High school degree, GED or equivalent 137 (20.7) 124 (20.8) 13 (20.0)  
 Some college, no degree, and above 407 (61.6) 368 (61.7) 39 (60.0)  
 Missing 3 (0.5)      
a

High perceived stress was defined as having a PSS T score of equal to or greater than 60. Medium/low was defined as having a PSS value below 60.

CpG site analysis

We used adjusted linear regression models to evaluate the association between continuous and binary prenatal perceived stress and DNAm measured in newborn blood samples at each of the 71 CpG sites located in the target genes measured on both the EPIC and 450K platforms (Supplementary Table 3; volcano plot is shown in Fig. 1). We observed suggestive associations (P < .05) at seven CpG sites located in the NR3C1 and FKBP5 genes (Table 2). At the top site, prenatal perceived stress levels were significantly (P < .0007) associated with blood DNAm at probe cg06613263 annotated to the NR3C1 gene, located in the gene body in the North Shore region within 2 kb upstream of the CpG island (Table 2). We observed a 0.021% increase in DNAm for every one-unit increase in prenatal perceived stress (P-value = .00027). Cg06613263 also emerged as the top site when perceived stress was treated as a binary variable (Supplementary Table 4). We observed a 0.27% (P-value = .011) increase in DNAm at cg06613263 in newborns whose mothers had high perceived stress levels over those whose mothers had low or medium perceived stress levels (Table 2).

Figure 1.

Figure 1.

Volcano plot of association testing results for prenatal perceived stress and newborn blood DNAm in NR3C1, FKBP5, and HSD11B2. Each point represents a CpG site. The dashed line represents the Bonferroni-corrected significance threshold (P < .0007).

Table 2.

Association between prenatal perceived stress and newborn blood DNAm levels at P < .05.

Probe ID Gene symbol Effecta SEa P-Valuea BH-FDR adjusted P-valuea % DNAm differencea
EPIC and 450K sites (n = 71 CpGs measured); N = 661 samples
Continuous PSS cg06613263 NR3C1 0.0050 0.0014 .00027 .019 0.021%
  cg00610228 FKBP5 0.0042 0.0018 .016 .408 0
  cg18849621 NR3C1 −0.0033 0.0014 .020 .408 −0.0069
  cg18019515 NR3C1 −0.0030 0.0013 .025 .408 0
  cg00862770 FKBP5 −0.0030 0.0014 .030 .408 −0.0069
  cg06087101 FKBP5 0.0061 0.0029 .035 .408 0.069
  cg14558428 NR3C1 −0.0030 0.0014 .040 .409 0
Binary PSS (65 high PSS group) cg06613263 NR3C1 0.074 0.029 .011 .484 0.27
  cg07733851 NR3C1 0.086 0.035 .014 .484 0.86
  cg16545496 HSD11B2 −0.063 0.028 .024 .576 −0.042
  cg18849621 NR3C1 −0.061 0.031 .051 .781 −0.15
EPIC only sites (66 CpGs measured); N = 137 samples
Continuous PSS cg24052866 NR3C1 0.0082 0.0026 .0015 .102 0.05910886
  cg25579735 NR3C1 −0.0061 0.0025 .015 .316 −0.0228306
  cg06409316 FKBP5 −0.0068 0.0029 .021 .316 −0.0453399
  cg24801588 NR3C1 −0.0058 0.0025 .022 .316 0.04393455
  cg13514002 NR3C1 −0.0040 0.0019 .032 .316 −0.0509034
  cg07633853 FKBP5 0.0052 0.0024 .033 .316 −0.013942
  cg21517946 FKBP5 −0.036 0.017 .034 .316 0.03 516 776
  cg14438279 NR3C1 −0.0043 0.0021 .043 .556 −0.1492263
a

Adjusted for maternal age at delivery, maternal depression, prenatal alcohol consumption, prenatal tobacco use, maternal education, and child’s sex.

Note: The coefficients and P-values were generated based on methylation M-value. %DNAm difference was generated based on methylation beta value.

We also performed analyses to evaluate the association between maternal perceived stress during pregnancy and DNAm in each of the 66 CpG sites specific to the EPIC array (Supplementary Table 5). Eight of these were nominally associated with continuous prenatal perceived stress T score levels (Table 2). We observed decreased neonatal blood DNAm with increased prenatal perceived stress at all but the top site where blood DNAm increased with increased perceived stress (cg24052866 annotated to NR3C1, % change = 0.059%, P-value = .0015). However, none of these associations met a conservative Bonferroni threshold correcting for multiple testing.

In sex-stratified analyses, cg06613262 was also the top site in male only models where we observed a nominally significant association between DNAm and prenatal perceived stress (% difference = 0.028% per one-unit increase in prenatal perceived stress, P-value = .0029) (Supplementary Table 6). In female only models, we similarly observed a suggestive association at this site (% difference = 0.014% per one-unit increase in prenatal perceived stress, P-value = .031). In statistical interaction models, we found no evidence of interaction by sex at this site (Pinteraction value = .33). However, the lowest P-value was observed at cg07724674 annotated to the HSD11B2 gene (% difference = 0.021% per one-unit increase in prenatal perceived stress, P-value = .00096) (Supplementary Table 7). In male children, the association between maternal perceived stress during pregnancy and newborn DNAm was not significant and showed an opposite direction of effect at this site (% difference = −0.0069% per one-unit increase in prenatal perceived stress, P-value = .358). Additionally, statistical interaction models showed evidence of interaction by sex at this site (Pinteraction value = .069).

Sensitivity analysis

Sensitivity analyses were carried out to examine the effect of preterm birth or increased familial predisposition to autism on the association between prenatal perceived stress and newborn blood DNAm at cg06613262. These results are presented in Table 3. Across all models, effect estimates did not vary largely from that obtained in the main, fully adjusted model, though the model that excluded participants from an ECHO site that enrolled participants with high familial autism predisposition produced a smaller % difference in blood DNAm with increased perceived stress (% DNAm change per one-unit increase on perceived stress = 0.014%, P-value = .012) compared to the full model.

Table 3.

Sensitivity analyses showing the association between prenatal perceived stress and newborn blood DNAm levels, at probe cg06613263 (NR3C1).

Analysis Sample size Effect Standard error P-value BH-FDR adjusted P-valuea % DNAm difference
Main analysis 661 0.0050 0.0014 .00027 .019 0.021%
≥37 weeks gestation 632 0.0045 0.0015 .0025 .199 0.021%
Excluding autism cohort site 637 0.0038 0.0015 .012 .257 0.014%
Excluding maternal prenatal depression from statistical model 661 0.0027 0.0010 .009 .312 0.007%
a

Adjusted for maternal age at delivery, maternal depression, prenatal alcohol consumption, prenatal tobacco use, maternal education, and child’s sex.

Note: The coefficients and P-values were generated based on methylation M-value. %DNAm difference was generated based on methylation beta value.

Additionally, we conducted sensitivity analyses to evaluate the effect of removing maternal prenatal depressive symptoms from our models assessing the association between prenatal perceived stress and newborn blood DNAm at cg06613262 (Table 3). We found a positive correlation between prenatal perceived stress and maternal prenatal depressive symptoms (r = 0.38, P-value < .001). Excluding maternal prenatal depressive symptoms from our models resulted in a smaller % difference in newborn blood DNAm with increased perceived stress (% DNAm change per one-unit increase on perceived stress = 0.007% P-value = .009) compared to the fully adjusted model, though the direction of effect remains consistent.

Gene-level tests

Mean methylation burden tests and SKAT were used to examine the association between prenatal perceived stress and offspring DNAm in each of four regions: (1) NR3C1, (2) FKBP5, (3) HSD11B2, and (4) all three genes together.

Mean methylation burden test

We calculated mean methylation for each participant within each gene region outlined above using the set of overlapping CpG sites between the 450K and EPIC arrays. A breakdown of each region and corresponding CpG sites is shown in Supplementary Table 8. We regressed mean DNAm in each region onto continuous perceived stress using fully adjusted linear regression models and found no evidence of association (Table 4). Models using mean methylation values calculated from EPIC-only CpG sites similarly returned null results (Supplementary Table 9).

Table 4.

Prenatal perceived stress and newborn mean methylation from shared CpG sites association testing results.

Gene symbol Number of sites β (95% confidence interval) a P-valuea
NR3C1 33 −0.0001 (−0.0010, 0.0007) .79
FKBP5 26 0.0001 (−0.0008, 0.0010) .81
HSD11B2 12 0.0004 (−0.0008, 0.0015) .52
Overall 71 0.0000 (−0.0007, 0.0007) .97
a

Adjusted for maternal age at delivery, maternal depression, prenatal alcohol consumption, prenatal tobacco use, maternal education, and child’s sex.

SKAT

We then used SKAT, applying various kernel and weight combinations, to more flexibly model the association between aggregate newborn blood DNAm across overlapping 450K and EPIC CpG sites within each delineated region and prenatal perceived stress. These results are presented in Table 5. First, we used a linear kernel to model the additive effects of each CpG site and weighted all sites evenly (weights = 1 or unweighted). We observed a significant association between prenatal perceived stress and DNAm patterns in the NR3C1 (P-value = .040) and FKBP5 genes (P-value = .024), and across all 71 sites in the three HPA axis pathway genes (NR3C1, FKBP5, and HSD11B2) together (P-value = .022). Secondary analyses in which we applied a quadratic kernel to model potential interactions between sites yielded similar results, showing significant effects in NR3C1 (P-value = .040) and FKBP5 (P-value = .037), and the set of all sites across the three genes under study (P- value = .039). Weighting the models by effect estimates obtained in single-site analyses had no effect on the associations. Similar results were obtained when we restricted these analyses to the set of 66 CpG sites measured on the EPIC array only (Supplementary Table 10).

Table 5.

Continuous prenatal perceived stress and newborn DNAm gene-based SKAT results.

Linear unweighted Quadratic unweighted Linear weighted Quadratic weighted
Gene symbols Number of sites Q P-value Q P-value Q P-value Q P-value
NR3C1 33 609.68 .040 904 900.60 .040 609.68 .040 904 900.60 .040
FKBP5 26 613.45 .024 365 607.1 .037 613.45 .024 365 607.1 .037
HSD11B2 12 151.94 .14 63 388.65 .17 151.94 .14 63 388.65 .17
All sites 71 1375.07 .022 368 891.00 .039 1375.07 .022 368 891.00 .039

Note: Adjusted for maternal age at delivery, maternal depression, prenatal alcohol consumption, prenatal tobacco use, maternal education, and child’s sex.

Finally, to optimize between SKAT and burden test approaches, we reran SKAT using the SKAT-O or optimal test method using a linear kernel and weighting all sites equally (Supplementary Table 11). Resulting P-values were larger in all four regions compared with that produced in original SKAT analyses, with associations between prenatal perceived stress and DNAm in FKBP5 and across all sites only approaching significance (P-valueFKBP5 = .055, P-value All sites = .076). Correlations between CpG sites within each region were 0 for all but the HSD11B2 region where the correlation between sites was determined to be 0.75.

In sex-stratified analyses, aggregate newborn blood DNAm in the FKBP5 gene remained statistically significantly associated with prenatal perceived stress in female-only samples (P-value = .004), but not in male-only samples (P = .60) (Table 6). On the other hand, the association between DNAm in HSD11B2 and prenatal perceived stress showed stronger significance in male newborns (P-value = .064), compared to female newborns (P-value = .26).

Table 6.

Continuous prenatal perceived stress and newborn DNAm SKAT results (linear, unweighted) in female-only and male-only samples.

Female samples (N = 325) Male samples (N = 336)
Region Number of sites Q P-value Q P-value
NR3C1 33 107.26 .53 286.12 .22
FKBP5 26 345.45 .0042 153.66 .60
HSD11B2 12 46.21 .26 107.68 .074
All sites 71 498.92 .080 547.45 .28

Note: Adjusted for maternal age at delivery, maternal depression, prenatal alcohol consumption, prenatal tobacco use, and maternal education.

Discussion

Our findings contribute to the growing body of literature investigating the molecular processes involved in foetal response to maternal stress exposure during pregnancy. Prenatal stress has been linked to poor offspring physical and neurodevelopmental outcomes, though the underlying mechanisms remain unclear [7, 8]. Prior work has identified the HPA axis as a pathway of interest, and studies have examined associations between prenatal stress, largely focused on SLEs, and stress-related psychopathology like depression and anxiety. To our knowledge, this is one of the largest studies to date in a diverse US population that has examined the association between prenatal perceived stress and newborn DNAm in HPA axis-related genes (NR3C1, FKBP5, and HSD11B2) and one of the few that have examined potential sex differential effects in offspring.

In single-site analyses, we found evidence that higher prenatal perceived stress exposure on a continuous scale was associated with DNAm changes in various sites located in NR3C1 and FKBP5 genes. Specifically, maternal perceived stress during pregnancy was significantly associated with increased DNAm in cg06613263 located in the NR3C1 gene body in a CpG North Shore region. One prior study has identified an association between maternal financial difficulties at 8 months postnatal and offspring DNAm at this site at age 7 [57]. Similarly, when prenatal perceived stress was modelled as a binary exposure, high perceived stress during pregnancy was associated with increased offspring DNAm, compared to low and medium perceived stress, though this association was not significant after correcting for multiple testing. These results largely corroborate previous findings. Prior studies have reported associations between prenatal stressors (such as war-related stress, maternal depression, and anxiety) and newborn cord blood and placenta DNAm in NR3C1 CpG sites [24, 25, 32, 58]. A few studies, however, failed to find significant associations between prenatal maternal stress and newborn DNAm in this gene [26, 27]. Mansell et al. [27], e.g. found that while prenatal perceived stress was marginally associated with site-specific methylation in NR3C1 in infant cord blood, this association did not remain after correcting for multiple testing. This discrepancy in results may reflect lack of statistical power due to small sample sizes, differences in sites assessed and DNAm measurement methods, and differences in choice of covariates across studies.

In addition to single CpG analyses, a complementary gene-level test using both mean methylation burden tests and the SKAT method. SKAT facilitates a flexible modelling approach, overcoming the assumption that methylation at multiple CpGs shows similar magnitudes and directions of effect used in standard aggregate methylation tests. Single-site analyses provide high-resolution information of specific positions in the genome that are different among newborns of mothers who experienced different levels of perceived stress during pregnancy, which may be useful for downstream in vitro functional analyses and summary statistic gene-level meta-analytic approaches across future studies, e.g. comb-p [59]. Gene-level analyses provide a complementary approach because they can improve power to detect significant associations, given their reduced multiple testing burden compared to single CpG analyses, and because focusing on gene-level targets may provide broader mechanistic insight to inform gene-level intervention targets.

The two region-based methods employed in this study produced inconsistent results. In SKAT region-based analyses, we observed a significant association between prenatal perceived stress and newborn DNAm in NR3C1, FKBP5, and across the three genes together. However, mean methylation burden tests produced null results across all regions. Additionally, while single CpG site analyses identified statistically significant associations between prenatal perceived stress and newborn DNAm in NR3C1, there were no statistically significant sites in FKBP5. Monk et al. [31] showed that prenatal distress was associated with increased NR3C1, FKBP5, and HSD11B2 placental mean methylation using bivariate Spearman correlation, though failed to adjust for relevant covariates, introducing concerns about unmeasured confounding.

The discrepancy in results obtained in the current study likely stems from test characteristics. Mean methylation burden tests assume the same direction and a similar magnitude of effect across CpG sites, and so may result in loss of power and masking of associations [39]. However, variance components score tests, such as SKAT, allow for more flexible modelling of the aggregate effect of CpG sites in a region by assuming that each site is independent, resulting in gains in power and improved detection when sites are truly independent [39, 40, 56]. Therefore, our results suggest that sites across each region act independently with different directions and magnitudes of effect. Sensitivity analysis using the SKAT-O method substantiates these conclusions. The SKAT-O or optimal test creates the optimal linear combination of SKAT and burden tests to optimize power by determining and incorporating correlation between sites into statistical models [56]. In our analyses, SKAT-O results showed no correlation (⍴ = 0) in NR3C1 and HSD11B2 genes, indicating the SKAT method was optimal. This is in keeping with what we would expect biologically as CpG sites have different downstream effects that depend in part on where the site is located in the gene. For example, DNAm in the promoter region has been shown to be associated with transcriptional repression, and DNAm in gene bodies has been shown to result in transcriptional activation [60]. Furthermore, our finding that prenatal perceived stress was statistically significantly associated with newborn DNAm in FKBP5 in SKAT gene-level but not in single CpG site analysis may be attributed to power gained through this SKAT method.

Additionally, SKAT analyses using linear and quadratic kernel functions both revealed significant associations in FKBP5, suggesting both additive and synergistic effects between sites. However, given the smaller P-value obtained in the linear kernel model, there is greater statistical evidence in support of additive effects within these regions.

In sex-stratified analyses, the top site in female-only samples was located in HSD11B2 single-site analyses, while this site did not appear to be associated with maternal perceived stress during pregnancy in male-only samples. In sex-stratified SKAT models, prenatal perceived stress was most strongly associated with aggregate methylation in FKBP5 in females and HSD11B2 in males, though the association in males was only suggestive. While we found no prior evidence in the literature that showed that newborn FKBP5 methylation differences in response to prenatal maternal stress is more pronounced in female compared to male newborns, Appleton et al. [61] similarly showed that male infants had greater decreases in placental HSD11B2 mean methylation in response to lower maternal education, increased poverty, and increased maternal socioeconomic risk than female infants. Conversely, Sutherland et al. [62] showed that in girls only with low levels of placental DNAm in HSD11B2, increased prenatal maternal depressive symptoms were associated with increased infant baseline cortisol. Sex differences in newborn DNAm changes associated with maternal prenatal stress exposure are largely understudied. Evidence has highlighted sex differences in foetal development and suggests an increased susceptibility to an adverse early life environment among male compared to female foetuses [63]. Future work is needed to better evaluate the presence and mechanisms of timing and sex differences in newborn DNAm patterns in response to the prenatal environment.

The relatively large sample size (N = 661) and the inclusion of participants from traditionally underrepresented racial/ethnic groups are among the main strengths of this study, leading to gains in power and improved generalizability of study results to the general US population. Additionally, our relatively novel use of SKAT in gene-level tests allowed for more flexible modelling and gains in power that better enabled us to detect the aggregate effect of DNAm in CpG within a region over burden tests that has been used in previous studies.

This study also has some important limitations. Primarily, while we did our best to control for confounders, it is possible that other unmeasured covariates, which have not been accounted for in our models, may play some role in the association between prenatal perceived stress and newborn DNAm in glucocorticoid related genes. Measurement error may have been another limitation of this study, particularly for self-reported measures such as maternal alcohol consumption or tobacco use during pregnancy, potentially leading to based estimates. Additionally, it is possible that the association between maternal perceived stress during pregnancy and newborn DNAm may be modified by self-reported race, as experiences of stress among pregnant women have been shown to differ across sociodemographic categories, including race and ethnicity [35, 36]. However, given sample size limitations, we lacked the power to perform these sub-analyses. However, the primary goal of these analyses was to identify DNAm differences across racial/ethnic groups and so future well-powered studies that evaluate racial/ethnic differences may be valuable. It is also possible that the association varied across ECHO cohort sites, particularly given the difference in exposure distribution across sites. Due to insufficient sample sizes and inadequate power, we were unable to conduct cohort-specific analyses and elucidate potential cohort effects. However, as cohort site coincided with technical batch, batch correction may have minimized the effect of between cohort differences on our results.

This study and others have largely focused on the role of maternal experiences of acute SLEs and stress appraisal during pregnancy or perceived stress. We compared aggregate DNAm analysis methods, specifically mean DNAm burden tests and our SKAT-based approach. Our results suggest key advantages of the SKAT method, including gains in power that allowed us to identify statistically significant associations between prenatal perceived stress and newborn DNAm in NR3C1 and FKBP5. These results suggest that future studies seeking to examine aggregate gene methylation associations with exposures or health outcomes would benefit from the use of SKAT over more traditional mean DNAm burden tests.

Future work should also explore other measures of stress, including cumulative or chronic stressors or biological stress correlates, such as cortisol, to better model the biological pathway between prenatal stress and offspring DNAm. Additionally, this study established an association between maternal perceived stress during pregnancy and newborn DNAm HPA axis-associated genes. As prior work has demonstrated connections between maternal perceived stress during pregnancy and offspring health outcomes, future work that evaluates whether the DNAm changes we identified mediate specific perinatal and child health outcomes is necessary. Finally, future studies should explore the potential impact of postnatal factors on offspring DNAm in order to identify potential intervention measures.

Supplementary Material

dvaf024_Supplemental_File

Acknowledgements

The authors wish to thank our ECHO colleagues; the medical, nursing, and program staff; and the children and families participating in the ECHO cohort. The ECHO-wide Cohort Data Collection Protocol was approved by the central ECHO institutional review board (IRB) or by individual cohorts’ IRBs of record. Study protocols were approved by the individual Institutional Review Boards at each site. Written informed consent or parent’s/guardian’s permission was obtained along with child assent as appropriate for ECHO-wide Cohort Data Collection Protocol participation and for participation in specific cohorts.

Appendix

Table A.1.

Overview of Notation.

First Name and Middle Initial(s) Last Name Suffix (e.g., Jr, III) Academic Degrees Department Institution Location (city, state/province, country) Role or Contribution ECHO Cohort Study Site or Core Name and Grant Number Email Address
P Brian Smith   MD, MPH, MHS Division of Neonatology, Department of Pediatrics Duke Clinical Research Institute, Duke University School of Medicine Durham, North Carolina, USA ECHO Coordinating Center Principal Investigator U2COD023375 (Coordinating Center) brian.smith@duke.edu
L Kristin Newby   MD, MHS Division of Cardiology, Department of Medicine Duke Clinical Research Institute, Duke University School of Medicine Durham, North Carolina, USA ECHO Coordinating Center Principal Investigator U2COD023375 (Coordinating Center) kristin.newby@duke.edu
Linda Adair   PhD Department of Nutrition Gillings School of Global Public Health, University of North Carolina at Chapel Hill Chapel Hill, North Carolina, USA ECHO Coordinating Center Principal Investigator U2COD023375 (Coordinating Center) linda_adair@unc.edu
Lisa P. Jacobson   ScD Department of Epidemiology Johns Hopkins University, Bloomberg School of Public Health Baltimore, Maryland, USA ECHO Data Analysis Center Principal Investigator U24OD023382 (Data Analysis Center) ljacobs1@jhu.edu
Diane Catellier   DrPH N/A Research Triangle Institute Research Triangle Park, North Carolina, USA ECHO Data Analysis Center Principal Investigator U24OD023382 (Data Analysis Center) dcatellier@rti.org
Monica McGrath   ScD Department of Epidemiology Johns Hopkins University, Bloomberg School of Public Health Baltimore, Maryland, USA ECHO Johns Hopkins University Data Analysis Center Director Co-Investigator U24OD023382 (Data Analysis Center) mmcgrat4@jhu.edu
Christian Douglas   DrPH N/A Research Triangle Institute Research Triangle Park, North Carolina, USA ECHO RTI Data Analysis Center Director Co-Investigator U24OD023382 (Data Analysis Center) christiand@rti.org
Priya Duggal   PhD Department of Epidemiology Johns Hopkins University, Bloomberg School of Public Health Baltimore, Maryland, USA ECHO Data Analysis Center Genetics Methods Lead, Co-Investigator U24OD023382 (Data Analysis Center) pduggal@jhu.edu
Emily Knapp   PhD Department of Epidemiology Johns Hopkins University, Bloomberg School of Public Health Baltimore, Maryland, USA ECHO Data Analysis Center Co-Investigator U24OD023382 (Data Analysis Center) eknapp2@jhu.edu
Amii Kress   PhD Department of Epidemiology Johns Hopkins University, Bloomberg School of Public Health Baltimore, Maryland, USA ECHO Data Analysis Center General Methods Co-Investigator U24OD023382 (Data Analysis Center) akress1@jhu.edu
Courtney K. Blackwell   PhD Department of Medical Social Sciences Feinberg School of Medicine, Northwestern University Chicago, Illinois, USA Measurement Core Co-Investigator U24OD023319 with co-funding from the Office of Behavioral and Social Science Research (Measurement Core) Ckblackwell@northwestern.edu
Maxwell A. Mansolf   PhD Department of Medical Social Sciences Feinberg School of Medicine, Northwestern University Chicago, Illinois, USA Measurement Core Co-Investigator U24OD023319 with co-funding from the Office of Behavioral and Social Science Research (Measurement Core) maxwell.mansolf@northwestern.edu
Jin-Shei Lai   PhD Department of Medical Social Sciences Feinberg School of Medicine, Northwestern University Chicago, Illinois, USA Measurement Core Co-Investigator U24OD023319 with co-funding from the Office of Behavioral and Social Science Research (Measurement Core) js-lai@northwestern.edu
Emily Ho   PhD Department of Medical Social Sciences Feinberg School of Medicine, Northwestern University Chicago, Illinois, USA Measurement Core Co-Investigator U24OD023319 with co-funding from the Office of Behavioral and Social Science Research (Measurement Core) emily-ho@northwestern.edu
David Cella   PhD Department of Medical Social Sciences Feinberg School of Medicine, Northwestern University Chicago, Illinois, USA Measurement Core Principal Investigator U24OD023319 with co-funding from the Office of Behavioral and Social Science Research (Measurement Core) d-cella@northwestern.edu
Richard Gershon   PhD Department of Medical Social Sciences Feinberg School of Medicine, Northwestern University Chicago, Illinois, USA Measurement Core Principal Investigator U24OD023319 with co-funding from the Office of Behavioral and Social Science Research (Measurement Core) gershon@northwestern.edu
Michelle L. Macy   MD Department of Pediatrics Feinberg School of Medicine, Northwestern University and Ann & Robert H. Lurie Children's Hospital of Chicago Chicago, Illinois, USA Measurement Core Co-Investigator U24OD023319 with co-funding from the Office of Behavioral and Social Science Research (Measurement Core) mmacy@luriechildrens.org
Suman R. Das   PhD Division of Infectious Diseases, Department of Medicine Vanderbilt University Medical Center Nashville, Tennessee, USA ECHO Laboratory Core Principal Investigator U24OD035523 (Lab Core) suman.r.das@vumc.org
Jane E. Freedman   MD Division of Cardiovascular Medicine, Department of Medicine Vanderbilt University Medical Center Nashville, Tennessee, USA ECHO Laboratory Core Principal Investigator U24OD035523 (Lab Core) jane.freedman@vumc.org
Simon A. Mallal   MBBS Division of Infectious Diseases, Department of Medicine Vanderbilt University Medical Center Nashville, Tennessee, USA ECHO Laboratory Core Principal Investigator U24OD035523 (Lab Core) s.mallal@vumc.org
John A. McLean   PhD Department of Chemistry Vanderbilt University Nashville, Tennessee, USA ECHO Laboratory Core Principal Investigator U24OD035523 (Lab Core) john.a.mclean@vanderbilt.edu
Ravi V. Shah   MD Division of Cardiovascular Medicine, Department of Medicine Vanderbilt University Medical Center Nashville, Tennessee, USA ECHO Laboratory Core Principal Investigator U24OD035523 (Lab Core) ravi.shah@vumc.org
Meghan H. Shilts   MHS Division of Infectious Diseases, Department of Medicine Vanderbilt University Medical Center Nashville, Tennessee, USA ECHO Laboratory Core Principal Investigator Admin Designee U24OD035523 (Lab Core) meghan.h.shilts@vumc.org
Akram N. Alshawabkeh   PhD College of Engineering Northeastern University Boston, Massachusetts, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023251 (Akram Alshawabkeh) a.alshawabkeh@northeastern.edu
Jose F. Cordero   MD College of Public Health, Department of Epidemiology & Biostatistics University of Georgia Athens, Georgia; USA ECHO Cohort Study Site Co-Director UG3/UH3OD023251 (Akram Alshawabkeh) jcordero@uga.edu
John Meeker   ScD Environmental Health Sciences, School of Public Health University of Michigan Ann Arbor, Michigan; USA ECHO Cohort Study Site Co-Director UG3/UH3OD023251 (Akram Alshawabkeh) meekerj@umich.edu
Leonardo Trasande   MD, MPP Departments of Pediatrics and Population Health NYU Grossman School of Medicine New York, New York, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023305 (Leonardo Trasande) leonardo.trasande@nyulangone.org
Carlos A. Camargo Jr. MD, DrPH Department of Emergency Medicine Massachusetts General Hospital, Harvard Medical School Boston, Massachusetts, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023253 (Carlos Camargo) ccamargo@mgb.org
Kohei Hasegawa   MD, PhD Department of Emergency Medicine Massachusetts General Hospital, Harvard Medical School Boston, Massachusetts, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023253 (Carlos Camargo) khasegawa@mgh.harvard.edu
Zhaozhong Zhu   ScD Department of Emergency Medicine Massachusetts General Hospital, Harvard Medical School Boston, Massachusetts, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023253 (Carlos Camargo) zzhu5@mgh.harvard.edu
Ashley F. Sullivan   MS, MPH Department of Emergency Medicine Massachusetts General Hospital, Harvard Medical School Boston, Massachusetts, USA ECHO Cohort Study Site Award Project Director UG3/UH3OD023253 (Carlos Camargo) afsullivan@mgb.org
Dana Dabelea   MD, PhD Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center University of Colorado Anschutz Medical Campus Aurora, Colorado, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023248 and UG3OD035526 (Dana Dabelea) dana.dabelea@cuanschutz.edu
Wei Perng   PhD, MPH Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center University of Colorado Anschutz Medical Campus Aurora, Colorado, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023248 (Dana Dabelea) wei.perng@cuanschutz.edu
Traci A. Bekelman   PhD, MPH Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center University of Colorado Anschutz Medical Campus Aurora, Colorado, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023248 (Dana Dabelea) traci.bekelman@cuanschutz.edu
Greta Wilkening   PhD, MPH Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center University of Colorado Anschutz Medical Campus Aurora, Colorado, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023248 (Dana Dabelea) Greta.Wilkening@childrenscolorado.org
Sheryl Magzamen   PhD Environmental and Radiological Health Sciences Colorado School of Public Health, Colorado State University Fort Collins, Colorado, USA ECHO Cohort Study Site Co-Investigator UG3OD035526 (Dana Dabelea) Sheryl.Magzamen@colostate.edu
Brianna F. Moore   PhD, MS Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center University of Colorado Anschutz Medical Campus Aurora, Colorado, USA ECHO Cohort Study Site Principal Investigator UG3OD035526 (Dana Dabelea) brianna.f.moore@cuanschutz.edu
Anne P. Starling   PhD Epidemiology University of North Carolina at Chapel Hill Chapel Hill, North Carolina, USA ECHO Cohort Study Site Principal Investigator UG3OD035526 (Dana Dabelea) anne.starling@unc.edu
Deborah J. Rinehart   PhD Center for Health Systems Research Denver Health and Hospital Authority Denver, Colorado, USA ECHO Cohort Study Site Co-Investigator UG3OD035526 (Dana Dabelea) deborah.rinehart@dhha.org
Daphne Koinis Mitchell   Ph.D Department of Pediatrics Rhode Island Hospital, The Alpert Medical School of Brown University Providence, Rhode Island, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023313 (Daphne Koinis Mitchell) dkoinismitchell@lifespan.org
Viren D'Sa   MD Department of Pediatrics Rhode Island Hospital, The Alpert Medical School of Brown University Providence, Rhode Island, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023313 (Daphne Koinis Mitchell) viren_Dsa@brown.edu
Sean C.L. Deoni   PhD Division of Gender Equality, Maternal, Newborn & Child Health Discovery & Tools Team Bill & Melinda Gates Foundation Seattle, Washington, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023313 (Daphne Koinis Mitchell) Sean.Deoni@gatesfoundation.org
Hans-Georg Mueller   PhD Department of Statistics University of California, Davis Davis, California, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023313 (Daphne Koinis Mitchell) hgmueller@ucdavis.edu
Cristiane S. Duarte   PhD, MPH Division of Child and Adolescent Psychiatry Columbia University - NYSPI New York, New York, USA ECHO Cohort Study Site Principal Investigator UH3OD023328 (Cristiane Duarte) Cristiane.Duarte@nyspi.columbia.edu
Catherine Monk   PhD Department of Obstetrics & Gynecology Columbia University - NYSPI New York, New York, USA ECHO Cohort Study Site Principal Investigator UH3OD023328 (Cristiane Duarte) cem31@cumc.columbia.edu
Glorisa Canino   PhD Behavioral Sciences Research Institute University of Puerto Rico, School of Medicine Rio Piedras, Puerto Rico ECHO Cohort Study Site Principal Investigator UH3OD023328 (Cristiane Duarte) glorisa.canino@upr.edu
Jonathan Posner   MD Child & Family Mental Health & Community Psychiatry Division Duke University School of Medicine, Duke Psychiatry & Behavioral Sciences Durham, North Carolina, USA ECHO Cohort Study Site Principal Investigator UH3OD023328 (Cristiane Duarte) jonathan.posner@duke.edu
Tenneill Murray   MPH Division of Child and Adolescent Psychiatry Columbia University - NYSPI New York, New York, USA ECHO Cohort Study Site Co-Director UH3OD023328 (Cristiane Duarte) tenneill.murray@nyspi.columbia.edu
Claudia Lugo-Candelas   PhD Division of Child and Adolescent Psychiatry Columbia University - NYSPI New York, New York, USA ECHO Cohort Study Site Principal Investigator UH3OD023328 (Cristiane Duarte) claudia.lugo@nyspi.columbia.edu
Anne L. Dunlop   MD, MPH Department of Gynecology and Obstetrics Emory University School of Medicine Atlanta, Georgia, USA ECHO Cohort Study Site Principal Investigator UH3OD023318 (Anne Dunlop) amlang@emory.edu
Patricia A. Brennan   PhD Department of Psychology Emory University Atlanta, Georgia, USA ECHO Cohort Study Site Principal Investigator UH3OD023318 (Anne Dunlop) pbren01@emory.edu
Christine Hockett   PhD N/A; Department of Pediatrics Avera Research Institute; University of South Dakota School of Medicine Rapid City, South Dakota, USA; Sioux Falls, South Dakota, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023279 (Amy Elliott) christine.hockett@avera.org
Amy Elliott   PhD N/A; Department of Pediatrics Avera Research Institute ; University of South Dakota School of Medicine Sioux Falls, South Dakota, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023279 (Amy Elliott) amy.elliott@avera.org
Assiamira Ferrara   MD, PhD Division of Research Kaiser Permanente Northern California Oakland, California, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023289 (Assiamira Ferrara) assiamira.ferrara@kp.org
Lisa A. Croen   PhD Division of Research Kaiser Permanente Northern California Oakland, California, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023342 (Kristen Lyall), UG3/UH3OD023289 (Assiamira Ferrara) Lisa.A.Croen@kp.org
Monique M. Hedderson   PhD Division of Research Kaiser Permanente Northern California Oakland, California, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023289 (Assiamira Ferrara), UG3OD035540 (Monique Marie Hedderson) Monique.M.Hedderson@kp.org
John Ainsworth   PhD Centre for Health Informatics University of Manchester Manchester, United Kingdom ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) John.Ainsworth@manchester.ac.uk
Leonard B. Bacharier   MD Department of Pediatrics, Monroe Carell Jr Children’s Hospital at Vanderbilt Vanderbilt University Medical Center Nashville, Tennessee, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) leonard.bacharier@vumc.org
Casper G. Bendixsen   PhD National Farm Medicine Center Marshfield Clinic Research Institute Marshfield, Wisconsin, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) Bendixsen.casper@marshfieldresearch.org
James E. Gern   MD Department of Pediatrics University of Wisconsin School of Medicine and Public Health Madison, Wisconsin, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern), UG3OD035509 (Anne Marie Singh) gern@medicine.wisc.edu
Diane R. Gold   MD The Channing Division of Network Medicine; Department of Medicine Brigham and Women’s Hospital; Harvard Medical School Boston, Massachusetts, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) redrg@channing.harvard.edu
Tina V. Hartert   MD, MPH Division of Pediatric Allergy, Immunology, and Pulmonary Medicine, Department of Medicine, Department of Pediatrics Vanderbilt University Medical Center Nashville, Tennessee, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern), UG3OD035516 and UG3OD035517 (Tina Hartert) tina.hartert@vumc.org
Daniel J. Jackson   MD Department of Pediatrics University of Wisconsin School of Medicine and Public Health Madison, Wisconsin, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) djj@medicine.wisc.edu
Christine C. Johnson   PhD Department of Public Health Sciences Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern), UG3OD035518 (Jennifer Straughen) CJOHNSO1@hfhs.org
Christine L.M. Joseph   PhD Department of Public Health Sciences Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) cjoseph1@hfhs.org
Meyer Kattan   MD Department of Pediatrics Columbia University Medical Center New York, New York, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) mk2833@cumc.columbia.edu
Gurjit K. Khurana Hershey   MD, PhD Division of Asthma Research Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) gurjit.hershey@cchmc.org
Robert F. Lemanske, Jr.   MD Department of Pediatrics University of Wisconsin School of Medicine and Public Health Madison, Wisconsin, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) lemanske@wisc.edu
Susan V. Lynch   PhD Department of Medicine University of California San Francisco, California, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) Susan.Lynch@ucsf.edu
Rachel L. Miller   MD Department of Medicine; Division of Clinical Immunology Icahn School of Medicine at Mount Sinai New York, New York, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern), UG3/UH3OD023290 (Julie Herbstman) Rachel.miller2@mssm.edu
George T. O’Connor   MD Department of Pediatrics Boston University School of Medicine Boston, Massachusetts, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) goconnor@bu.edu
Carole Ober   PhD Department of Human Genetics University of Chicago Chicago, Illinois, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern), UG3OD035509 (Anne Marie Singh) c-ober@genetics.uchicago.edu
Dennis Ownby   MD Department of Public Health Sciences Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) downby@augusta.edu
Katherine Rivera-Spoljaric   MD Department of Pediatrics Washington University School of Medicine St Louis, Missouri, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern), UG3OD035521 (Katherine Rivera-Spoljaric) rivera_k@wustl.edu
Patrick H. Ryan   PhD Department of Pediatrics and College of Medicine; Division of Biostatistics and Epidemiology University of Cincinnati Cincinnati, Ohio, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern), UG3OD035509 (Anne Marie Singh) patrick.ryan@cchmc.org
Christine M. Seroogy   MD Department of Pediatrics University of Wisconsin School of Medicine and Public Health Madison, Wisconsin, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) cmseroogy@wisc.edu
Anne Marie Singh   MD Department of Pediatrics University of Wisconsin School of Medicine and Public Health Madison, Wisconsin, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern), UG3OD035509 (Anne Marie Singh) amsingh@wisc.edu
Robert A. Wood   MD Department of Pediatrics Johns Hopkins University School of Medicine Baltimore, Maryland, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern) rwood@jhmi.edu
Edward M. Zoratti   MD Division of Allergy and Clinical Immunology Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023282 (James Gern), UG3OD035518 (Jennifer Straughen) ezoratt1@hfhs.org
Rima Habre   ScD, MSc Department of Population and Public Health Sciences University of Southern California Los Angeles, California, USA ECHO Cohort Study Site Principal Investigator UH3OD023287 (Carrie Breton) habre@usc.edu
Shohreh Farzan   PhD Department of Population and Public Health Sciences University of Southern California Los Angeles, California, USA ECHO Cohort Study Site Principal Investigator UH3OD023287 (Carrie Breton) sffarzan@usc.edu
Frank D. Gilliland   MD, MPH, PhD Department of Population and Public Health Sciences University of Southern California Los Angeles, California, USA ECHO Cohort Study Site Principal Investigator UH3OD023287 (Carrie Breton) gillilan@usc.edu
Irva Hertz-Picciotto   PhD MIND Institute and Department of Public Health Sciences University of California, Davis Davis, California, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023365 (Irva Hertz-Picciotto), UG3OD035550 (Rebecca Schmidt) iher@ucdavis.edu
Deborah H. Bennett   Ph.D Department of Public Health Sciences University of California, Davis Davis, California, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023365 (Irva Hertz-Picciotto), UG3OD035550 (Rebecca Schmidt) dhbennett@ucdavis.edu
Julie B. Schweitzer   Ph.D Department of Psychiatry and Behavioral Science and the MIND Institute University of California, Davis Davis, California, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023365 (Irva Hertz-Picciotto) jschweitzer@ucdavis.edu
Rebecca J. Schmidt   Ph.D MIND Institute and Department of Public Health Sciences University of California, Davis Davis, California, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023365 (Irva Hertz-Picciotto), UG3/UH3OD023342 (Kristen Lyall), UG3OD035550 (Rebecca Schmidt) rjschmidt@ucdavis.edu
Janine M. LaSalle   PhD Medical Microbiology and Immunology; MIND Institute University of California, Davis Davis, California, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023365 (Irva Hertz-Picciotto), UG3OD035550 (Rebecca Schmidt) jmlasalle@ucdavis.edu
Alison E. Hipwell   PhD, ClinPsyD Psychiatry and Psychology University of Pittsburgh Pittsburgh, Pennsylvania, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023244 (Alison Hipwell) hipwae@upmc.edu
Kate E. Keenan   PhD Psychiatry and Behavioral Neuroscience University of Chicago Chicago, Illinois, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023244 (Alison Hipwell) kekeenan@uchicago.edu
Catherine J. Karr   MD, MS, PhD Department of Pediatrics, School of Medicine; Department of Environmental and Occupational Health Sciences; School of Public Health University of Washington Seattle, Washington, USA ECHO Cohort Study Site Principal Investigator UH3OD023271 and UG3OD035528 (Catherine Karr) ckarr@uw.edu
Nicole R. Bush   PhD Department of Psychiatry and Behavioral Sciences and Department of Pediatrics, School of Medicine University of California, San Francisco San Francisco, California, USA ECHO Cohort Study Site Principal Investigator UH3OD023271 (Catherine Karr), UG3OD035519 (Qi Zhao) nicole.bush@ucsf.edu
Kaja Z. LeWinn   ScD Department of Psychiatry and Behavioral Sciences, School of Medicine University of California, San Francisco San Francisco, California, USA ECHO Cohort Study Site Principal Investigator UH3OD023271 (Catherine Karr), UG3OD035519 (Qi Zhao) kaja.lewinn@ucsf.edu
Sheela Sathyanarayana   MD, MPH Department of Pediatrics, School of Medicine; Department of Environmental and Occupational Health Sciences, School of Public Health University of Washington and Seattle Children's Research Institute Seattle, Washington, USA ECHO Cohort Study Site Principal Investigator UH3OD023271 (Catherine Karr), UG3OD035508 (Sheela Sathyanarayana) sheela.sathyanarayana@seattlechildrens.org
Qi Zhao   MD, PhD Department of Preventive Medicine University of Tennessee Health Science Center Memphis, Tennessee, USA ECHO Cohort Study Site Principal Investigator UH3OD023271 (Catherine Karr), UG3OD035519 (Qi Zhao) qzhao11@uthsc.edu
Frances Tylavsky   DrPH, MS Department of Preventive Medicine University of Tennessee Health Science Center Memphis, Tennessee, USA ECHO Cohort Study Site Principal Investigator UH3OD023271 (Catherine Karr) ftylavsk@uthsc.edu
Kecia N. Carroll   MD, MPH Department of Pediatrics, Department of Environmental Medicine & Public Health Icahn School of Medicine at Mount Sinai New York, New York, USA ECHO Cohort Study Site Principal Investigator UH3OD023271 (Catherine Karr), UG3/UH3OD023337 (Rosalind Wright) kecia.carroll@mssm.edu
Christine T. Loftus   MS MPH PhD Department of Environmental and Occupational Health Sciences; School of Public Health University of Washington Seattle, Washington, USA ECHO Cohort Study Site Principal Investigator UH3OD023271 (Catherine Karr) cloftus@uw.edu
Leslie D. Leve   PhD Department of Counseling Psychology and Human Services & Prevention Science Institute University of Oregon Eugene, Oregon, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023389 (Leslie Leve) leve@uoregon.edu
Jody M. Ganiban   PhD Department of Psychological and Behavioral Sciences George Washington University Washington, DC, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023389 (Leslie Leve) ganiban@gwu.edu
Jenae M. Neiderhiser   PhD Department of Psychology Penn State University University Park, Pennsylvania, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023389 (Leslie Leve) jenaemn@psu.edu
Scott T. Weiss   MD Channing Division of Network Medicine, Department of Medicine Brigham and Women's Hospital and Harvard Medical School Boston, Massachusetts, USA ECHO Cohort Study Site Principal Investigator UH3OD023268 (Scott Weiss) scott.weiss@channing.harvard.edu
Augusto A. Litonjua   MD Pediatric Pulmonary Division, Department of Pediatrics Golisano Children's Hospital, University of Rochester Rochester, New York, USA ECHO Cohort Study Site Principal Investigator UH3OD023268 (Scott Weiss) augusto_litonjua@urmc.rochester.edu
Cindy T. McEvoy   MD, MCR Division of Neonatology, Department of Pediatrics Oregon Health & Science University Portland, Oregon, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023288 (Cynthia McEvoy) mcevoyc@ohsu.edu
Eliot R. Spindel   MD, PhD Division of Neuroscience Oregon National Primate Research Center Beaverton, Oregon, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023288 (Cynthia McEvoy) spindele@ohsu.edu
Robert S. Tepper   MD, PhD Division of Pediatric Pulmonology, Department of Pediatrics Indiana School of Medicine Indianapolis, Indiana, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023288 (Cynthia McEvoy) rtepper@iu.edu
Craig J. Newschaffer   PhD College of Health and Human Development Penn State State College, Pennsylvania, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023342 (Kristen Lyall) newschaffer@psu.edu
Kristen Lyall   ScD AJ Drexel Autism Institute Drexel University Philadelphia, Pennsylvania, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023342 (Kristen Lyall) kld98@drexel.edu
Heather E. Volk   PhD Mental Health Johns Hopkins University Baltimore, Maryland, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023342 (Kristen Lyall) hvolk1@jhu.edu
Rebecca Landa   PhD Department of Psychiatry and Behavioral Sciences Center for Autism and Related Disorders, Kennedy Krieger Institute, Johns Hopkins University Baltimore, Maryland, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023342 (Kristen Lyall) landa@kennedykrieger.org
Sally Ozonoff   PhD MIND Institute, Department of Psychiatry University of California Davis Sacramento, California, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023342 (Kristen Lyall) sozonoff@ucdavis.edu
Joseph Piven   MD Department of Psychiatry University of North Carolina Chapel Hill, North Carolina, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023342 (Kristen Lyall) jpiven@med.unc.edu
Heather Hazlett   PhD Department of Psychiatry University of North Carolina Chapel Hill, North Carolina, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023342 (Kristen Lyall) heather_cody@med.unc.edu
Juhi Pandey   PhD Center for Autism Research Children's Hospital of Philadelphia Philadelphia, Pennsylvania, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023342 (Kristen Lyall) pandeyj@chop.edu
Robert Schultz   PhD Center for Autism Research Children's Hospital of Philadelphia Philadelphia, Pennsylvania, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023342 (Kristen Lyall) schultzrt@chop.edu
Steven Dager   PhD Department of Radiology University of Washington Seattle, Washington, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023342 (Kristen Lyall) srd@uw.edu
Kelly Botteron   PhD Department of Psychiatry Washington University St Louis, Missouri, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023342 (Kristen Lyall) botteronk@wustl.edu
Daniel Messinger   PhD Department of Psychology University of Miami Miami, Florida, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023342 (Kristen Lyall) dmessinger@miami.edu
Wendy Stone   PhD Department of Psychology University of Washington Seattle, Washington, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023342 (Kristen Lyall) stonew@uw.edu
Jennifer Ames   PhD Kaiser Permanente Division of Research Kaiser Permanente Oakland, California, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023342 (Kristen Lyall) Jennifer.L.Ames@kp.org
Thomas G. O’Connor   PhD Departments of Psychiatry, Neuroscience, Obstetrics and Gynecology University of Rochester Rochester, New York, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023349 (Thomas O’Connor) tom_oconnor@urmc.Rochester.edu
Richard K. Miller   PhD Departments of Obstetrics and Gynecology University of Rochester Rochester, New York, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023349 (Thomas O’Connor) richardk_miller@urmc.rochester.edu
Emily Oken   MD, MPH Division of Chronic Disease Research Across the Lifecourse, Department of Population Medicine Harvard Pilgrim Health Care Institute and Harvard Medical School Boston, Massachusetts, USA ECHO Cohort Study Site Principal Investigator UH3OD023286 and UG3OD035533 (Emily Oken) emily_oken@hms.harvard.edu
Michele R. Hacker   ScD Department of Obstetrics and Gynecology Beth Israel Deaconess Medical Center Boston, Massachusetts, USA ECHO Cohort Study Site Principal Investigator UG3OD035533 (Emily Oken) mhacker@bidmc.harvard.edu
Tamarra James-Todd   PhD Department of Environmental Health Harvard Chan School of Public Health Boston, Massachusetts, USA ECHO Cohort Study Site Principal Investigator UG3OD035533 (Emily Oken) tjtodd@hsph.harvard.edu
T. Michael O'Shea Jr MD, MPH Division of Neonatology, Department of Pediatrics University of North Carolina School of Medicine Chapel Hill, North Carolina, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023348 (Mike O’Shea), UH3OD023347 (Barry Lester) moshea52@email.unc.edu
Rebecca C. Fry   PhD Department of Environmental Sciences and Engineering University of North Carolina Gillings School of Global Public Health Chapel Hill, North Carolina, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023348 (Mike O’Shea) rfry@unc.edu
Jean A. Frazier   MD EK Shriver Center and Psychiatry UMASS Chan Medical School Worcster, Massachusetts, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) jean.frazier@umassmed.edu
Rachana Singh   MD, MS Department of Pediatrics Tufts University School of Medicine Boston, Massachusetts, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) jean.frazier@umassmed.edu
Caitlin Rollins   MD, SM Department of Neurology Harvard Medical School Boston, Massachusetts, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) Rachana.Singh1@tuftsmedicine.org
Angela Montgomery   MD Division of Neonatology, Department of Pediatrics Yale School of Medicine New Haven, Connecticut, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) angela.montgomery@yale.edu
Ruben Vaidya   MD Department of Pediatrics University of Massachusetts Chan Medical School-Baystate Springfield, Massachusetts, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) Ruben.VaidyaMD@baystatehealth.org
Robert M. Joseph   PhD Department of Anatomy & Neurobiology Boston University Chobanian & Avedisian School of Medicine Boston, Massachusetts, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) rmjoseph@bu.edu
Lisa K. Washburn   MD Pediatrics Wake Forest School of Medicine Winston-Salem, North Carolina, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) lwcadmus@gmail.com
Semsa Gogcu   MD, MPH Section of Neonatology, Department of Pediatrics; Department of Pediatrics Wake Forest School of Medicine; Wake Forest University School of Medicine/Atrium Health Wake Forest Winston-Salem, North Carolina, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea), UG3OD035513 (Annemarie Stroustrup), UH3OD023320 (Judy Aschner) sgogcu@wakehealth.edu
Kelly Bear   DO Section of Neonatology, Department of Pediatrics ECU Health Greenville, North Carolina, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) BEARK17@ECU.EDU
Julie V. Rollins   MA Division of Neonatology, Department of Pediatrics University of North Carolina School of Medicine Chapel Hill, North Carolina, USA ECHO Cohort Study Site Award Project Director UG3/UH3OD023348 (Mike O’Shea) julie.rollins@unc.edu
Stephen R. Hooper   PhD Department of Health Sciences School of Medicine, University of North Carolina at Chapel Hill Chapel Hill, North Carolina, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) stephen_hooper@med.unc.edu
Genevieve Taylor   MD Pediatrics School of Medicine, University of North Carolina at Chapel Hill Chapel Hill, North Carolina, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) gtaylor@med.unc.edu
Wesley Jackson   MD, MPH Division of Neonatology, Department of Pediatrics University of North Carolina School of Medicine Chapel Hill, North Carolina, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) wesley.jackson@unc.edu
Amanda Thompson   PhD Department of Anthropology, Department of Nutrition University of North Carolina at Chapel Hill; Gillings School of Global Public Health, University of North Carolina at Chapel Hill Chapel Hill, North Carolina, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) althomps@email.unc.edu
Julie Daniels   PhD Epidemiology and Maternal and Child Health University of North Carolina at Chapel Hill; Gillings School of Global Public Health, University of North Carolina at Chapel Hill Chapel Hill, North Carolina, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) julie_daniels@unc.edu
Michelle Hernandez   MD Pediatrics School of Medicine, University of North Carolina at Chapel Hill Chapel Hill, North Carolina, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) michelle_hernandez@med.unc.edu
Kun Lu   PhD Environmental Sciences and Engineering Gillings School of Global Public Health, University of North Carolina at Chapel Hill Chapel Hill, North Carolina, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) kunlu@unc.edu
Michael Msall   MD Kennedy Research Center on Intellectual and Neurodevelopmental Disabilities University of Chicago Medicine: Comer Children's Hospital Chicago Illinois, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) mmsall@peds.bsd.uchicago.edu
Madeleine Lenski   MSPH Department of Epidemiology and Biostatistics Michigan State University East Lansing, Michigan, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) lenskim@msu.edu
Rawad Obeid   MD Pediatrics Beaumont Hospital Royal Oak, Michigan, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) Rawad.Obeid@beaumont.org
Steven L. Pastyrnak   PhD Pediatrics Corewell Health, Helen DeVos Children's Hospital Grand Rapids, Michigan, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea), UH3OD023347 (Barry Lester) Steve.Pastyrnak@helendevoschildrens.org
Elizabeth Jensen   PhD Epidemiology and Prevention Wake Forest University School of Medicine Winston-Salem, North Carolina, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) ejensen@wakehealth.edu
Christina Sakai   MD Pediatrics Mass General Hospital for Children Boston, Massachusetts, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023348 (Mike O’Shea) Christina.sakai@gmail.com
Hudson Santos   RN, PhD Dean's Office Graduate School, School of Nursing and Health Studies University of Miami Coral Gables, Florida, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023348 (Mike O’Shea), UG3OD035542 (Hudson Santos) hsantos@miami.edu
Jean M. Kerver   PhD, MSc, RD Departments of Epidemiology & Biostatistics, and Pediatrics & Human Development Michigan State University, College of Human Medicine East Lansing, Michigan, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023285 (Jean Kerver) kerverje@msu.edu
Nigel Paneth   MD, MPH Departments of Epidemiology & Biostatistics, and Pediatrics & Human Development Michigan State University, College of Human Medicine East Lansing, Michigan, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023285 (Jean Kerver) paneth@msu.edu
Charles J. Barone II MD, FAAP Department of Pediatrics Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023285 (Jean Kerver), UG3/UH3OD023282 (James Gern) cbarone1@hfhs.org
Michael R. Elliott   PhD Department of Biostatistics University of Michigan Ann Arbor, Michigan, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023285 (Jean Kerver) mrelliot@umich.edu
Douglas M. Ruden   PhD Department of Obstetrics and Gynecology, Institute of Environmental Health Sciences (IEHS), C.S. Mott Center for Human Health and Development Wayne State University Detroit, Michigan, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023285 (Jean Kerver) douglasr@wayne.edu
Chris Fussman   MS Lifecourse Epidemiology and Genomics Division Michigan Department of Health and Human Services (MDHHS) Lansing, Michigan, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023285 (Jean Kerver) fussmanc@michigan.gov
Julie B. Herbstman   PhD Department of Environmental Health Sciences Columbia University Mailman School of Public Health New York, New York, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023290 (Julie Herbstman) jh2678@cumc.columbia.edu
Amy Margolis   PhD Department of Psychiatry Columbia University Irving Medical Center New York, New York, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023290 (Julie Herbstman) amy.margolis@nyspi.columbia.edu
Susan L. Schantz   PhD Beckman Institute for Advanced Science and Technology; Department of Comparative Biosciences University of Illinois Urbana-Champaign Urbana, Illinois, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023272 (Susan Schantz) schantz@illinois.edu
Sarah Dee Geiger   PhD Beckman Institute for Advanced Science and Technology; Department of Kinesiology and Community Health University of Illinois Urbana-Champaign Urbana, Illinois, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023272 (Susan Schantz) smurphy7@illinois.edu
Andrea Aguiar   PhD Beckman Institute for Advanced Science and Technology; Department of Comparative Biosciences University of Illinois Urbana-Champaign Urbana, Illinois, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023272 (Susan Schantz) aaguiar@illinois.edu
Karen Tabb   PhD, MSW Beckman Institute for Advanced Science and Technology; Department of Social Work University of Illinois Urbana-Champaign Urbana, Illinois, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023272 (Susan Schantz) ktabb@illinois.edu
Rita Strakovsky   PhD Department of Food Science and Human Nutrition Michigan State University East Lansing, Michigan, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023272 (Susan Schantz) strakovs@msu.edu
Tracey Woodruff   PhD, MPH Program on Reproductive Health and the Environment University of California, San Francisco San Francisco, California, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023272 (Susan Schantz) tracey.woodruff@ucsf.edu
Rachel Morello-Frosch   PhD, MPH Department of Environmental Science, Policy and Management and School of Public Health University of California, Berkeley Berkeley, California, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023272 (Susan Schantz) rmf@berkeley.edu
Amy Padula   PhD Program on Reproductive Health and the Environment University of California, San Francisco San Francisco, California, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023272 (Susan Schantz) amy.padula@ucsf.edu
Joseph B. Stanford   MD, MSPH Department of Family and Preventive Medicine Spencer Fox Eccles School of Medicine, University of Utah Salt Lake City, Utah, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023249 (Joseph Stanford) joseph.stanford@utah.edu
Christina A. Porucznik   PhD, MSPH Department of Family and Preventive Medicine Spencer Fox Eccles School of Medicine, University of Utah Salt Lake City, Utah, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023249 (Joseph Stanford) christy.porucznik@utah.edu
Angelo P. Giardino   MD, PhD Department of Pediatrics Spencer Fox Eccles School of Medicine, University of Utah Salt Lake City, Utah, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023249 (Joseph Stanford) giardino@hsc.utah.edu
Rosalind J. Wright   MD, MPH Department of Environmental Medicine & Public Health Icahn School of Medicine at Mount Sinai New York, New York, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023337 (Rosalind Wright) rosalind.wright@mssm.edu
Robert O. Wright   MD, MPH Department of Environmental Medicine & Public Health Icahn School of Medicine at Mount Sinai New York, New York, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023337 (Rosalind Wright) robert.wright@mssm.edu
Brent Collett   PhD Department of Psychiatry and Behavioral Medicine University of Washington, Seattle Children's Research Institute Seattle, Washington, USA ECHO Cohort Study Site Principal Investigator UG3OD035508 (Sheela Sathyanarayana) brent.collett@seattlechildrens.org
Nicole Baumann-Blackmore   MD Department of Pediatrics University of Wisconsin School of Medicine and Public Health Madison, Wisconsin, USA ECHO Cohort Study Site Co-Investigator UG3OD035509 (Anne Marie Singh) nlbaumann@wisc.edu
Ronald Gangnon   PhD Department of Population Health Sciences University of Wisconsin Madison, Wisconsin, USA ECHO Cohort Study Site Co-Investigator UG3OD035509 (Anne Marie Singh) ronald@biostat.wisc.edu
Daniel J. Jackson   MD Department of Pediatrics University of Wisconsin School of Medicine and Public Health Madison, Wisconsin, USA ECHO Cohort Study Site Co-Investigator UG3OD035509 (Anne Marie Singh) djj@medicine.wisc.edu
Chris G. McKennan   PhD Department of Statistics University of Pittsburgh Pittsburgh, Pennsylvania, USA ECHO Cohort Study Site Co-Investigator UG3OD035509 (Anne Marie Singh) CHM195@pitt.edu
Jo Wilson   MD Department of Pediatrics University of Wisconsin School of Medicine and Public Health Madison, Wisconsin, USA ECHO Cohort Study Site Co-Investigator UG3OD035509 (Anne Marie Singh) wilson54@wisc.edu
Matt Altman   MD Department of Medicine University of Washington Seattle, Washington, USA ECHO Cohort Study Site Co-Investigator UG3OD035509 (Anne Marie Singh) maltman@benaroyaresearch.org
Judy L. Aschner   MD Department of Pediatrics Albert Einstein College of Medicine; Hackensack Meridian School of Medicine; Center for Discovery and Innovation Bronx, New York, USA; Nutley, New Jersey, USA ECHO Cohort Study Site Principal Investigator UH3OD023320 and UG3OD035546 (Judy Aschner), UG3OD035513 (Annemarie Stroustrup) judy.aschner@einsteinmed.edu; judy.aschner@hmhn.org
Annemarie Stroustrup   MD, MPH Department of Pediatrics Northwell Health, Cohen Children's Medical Center, and the Zucker School of Medicine at Hofstra / Northwell New Hyde Park, New York, USA ECHO Cohort Study Site Principal Investigator UH3OD023320 (Judy Aschner), UG3OD035513 (Annemarie Stroustrup) astroustrup@northwell.edu
Stephanie L. Merhar   MD, MS Department of Pediatrics Cincinnati Children's Cincinnati, Ohio, USA ECHO Cohort Study Site Co-Investigator UH3OD023320 (Judy Aschner), UG3OD035513 (Annemarie Stroustrup) stephanie.merhar@cchmc.org
Paul E. Moore   MD Department of Pediatrics Vanderbilt University Medical Center Nashville, Tennessee, USA ECHO Cohort Study Site Co-Investigator UH3OD023320 (Judy Aschner), UG3OD035513 (Annemarie Stroustrup) paul.moore@vumc.org
Gloria S. Pryhuber   MD Department of Pediatrics University of Rochester Medical Center Rochester, New York, USA ECHO Cohort Study Site Co-Investigator UH3OD023320 (Judy Aschner) gloria_pryhuber@urmc.rochester.edu
Mark Hudak   MD Department of Pediatrics University of Florida College of Medicine Jacksonville, Florida, USA ECHO Cohort Study Site Co-Investigator UH3OD023320 (Judy Aschner) mark.hudak@jax.ufl.edu
Ann Marie Reynolds Lyndaker   MD, MPH Department of Pediatrics University of Buffalo Jacobs School of Medicine and Biomedical Sciences Buffalo, New York, USA ECHO Cohort Study Site Co-Investigator UH3OD023320 (Judy Aschner) amr1@buffalo.edu
Andrea L. Lampland   MD Department of Pediatrics Children's Minnesota Minneapolis, Minnesota, USA ECHO Cohort Study Site Co-Investigator UH3OD023320 (Judy Aschner) andrea.lampland@childrensms.org
Burton Rochelson   MD Department of Obstetrics and Gynecology Northwell Health and the Zucker School of Medicine at Hofstra / Northwell New Hyde Park, New York, USA ECHO Cohort Study Site Principal Investigator UG3OD035532 (Annemarie Stroustrup) brochels@northwell.edu
Sophia Jan   MD, MSHP Department of Pediatrics Northwell Health, Cohen Children's Medical Center, and the Zucker School of Medicine at Hofstra / Northwell New Hyde Park, New York, USA ECHO Cohort Study Site Co-Investigator UG3OD035532 (Annemarie Stroustrup) sjan1@northwell.edu
Matthew J. Blitz   MD, MBA Department of Obstetrics and Gynecology Northwell Health and the Zucker School of Medicine at Hofstra / Northwell New Hyde Park, New York, USA ECHO Cohort Study Site Co-Investigator UG3OD035532 (Annemarie Stroustrup) mblitz@northwell.edu
Michelle W. Katzow   MD, MS Department of Pediatrics Northwell Health, Cohen Children's Medical Center, and the Zucker School of Medicine at Hofstra / Northwell New Hyde Park, New York, USA ECHO Cohort Study Site Co-Investigator UG3OD035532 (Annemarie Stroustrup) mkatzow@northwell.edu
Zenobia Brown   MD, MPH Department of Science Education Northwell Health and the Zucker School of Medicine at Hofstra / Northwell New Hyde Park, New York, USA ECHO Cohort Study Site Co-Investigator UG3OD035532 (Annemarie Stroustrup) zbrown2@northwell.edu
Codruta Chiuzan   PhD Institute of Health System Science Northwell Health, Feinstein Institutes for Medical Research Manhasset, New York, USA ECHO Cohort Study Site Co-Investigator UG3OD035532 (Annemarie Stroustrup) cchiuzan@northwell.edu
Timothy Rafael   MD Department of Obstetrics and Gynecology Northwell Health and the Zucker School of Medicine at Hofstra / Northwell New Hyde Park, New York, USA ECHO Cohort Study Site Co-Investigator UG3OD035532 (Annemarie Stroustrup) trafael@northwell.edu
Dawnette Lewis   MD, MPH Department of Obstetrics and Gynecology Northwell Health and the Zucker School of Medicine at Hofstra / Northwell New Hyde Park, New York, USA ECHO Cohort Study Site Co-Investigator UG3OD035532 (Annemarie Stroustrup) dlewis@northwell.edu
Natalie Meirowitz   MD Department of Obstetrics and Gynecology Northwell Health and the Zucker School of Medicine at Hofstra / Northwell New Hyde Park, New York, USA ECHO Cohort Study Site Co-Investigator UG3OD035532 (Annemarie Stroustrup) nmeirowi@northwell.edu
Brenda Poindexter   MD Department of Pediatrics Children's Healthcare of Atlanta Emory University Atlanta, Georgia, USA ECHO Cohort Study Site Co-Investigator UH3OD023320 (Judy Aschner) breda.pointdexter@emory.edu
Tebeb Gebretsadik   MPH Department of Biostatistics Vanderbilt University Medical Center Nashville, Tennessee, USA ECHO Cohort Study Site Principal Investigator UG3OD035516 and UG3OD035517 (Tina Hartert) tebeb.gebretsadik@vumc.org
Sarah Osmundson   MD, MSC Department of Obstetrics and Gynecology Vanderbilt University Medical Center Nashville, Tennessee, USA ECHO Cohort Study Site Principal Investigator UG3OD035517 (Tina Hartert) sarah.osmundson@vumc.org
Jennifer K. Straughen   PhD Department of Public Health Sciences Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Principal Investigator UG3OD035518 (Jennifer Straughen) jstraug1@hfhs.org
Amy Eapen   MD Division of Allergy and Clinical Immunology Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Principal Investigator UG3OD035518 (Jennifer Straughen) aeapen1@hfhs.org
Andrea Cassidy-Bushrow   PhD Department of Public Health Sciences Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023282 (James Gern) acassid1@hfhs.org
Ganesa Wegienka   PhD Department of Public Health Sciences Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023282 (James Gern) gwegien1@hfhs.org
Alex Sitarik   MPH Department of Public Health Sciences Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Biostatistician UG3/UH3OD023282 (James Gern) asitari1@hfhs.org
Kim Woodcroft   PhD Department of Public Health Sciences Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Co-Investigator UG3OD035518 (Jennifer Straughen), UG3/UH3OD023282 (James Gern) kwoodcr1@hfhs.org
Audrey Urquhart   MPH Department of Public Health Sciences Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Epidemiologist UG3OD035518 (Jennifer Straughen), UG3/UH3OD023282 (James Gern) aurquha1@hfhs.org
Albert Levin   PhD Department of Public Health Sciences Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Co-Investigator UG3OD035518 (Jennifer Straughen) alevin1@hfhs.org
Tisa Johnson-Hooper   MD Department of Pediatrics Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Co-Investigator UG3OD035518 (Jennifer Straughen) tjohnso2@hfhs.org
Brent Davidson   MD Department of Women's Health Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023282 (James Gern) bdavids1@hfhs.org
Tengfei Ma   PhD Department of Public Health Sciences Henry Ford Health Detroit, Michigan, USA ECHO Cohort Study Site Co-Investigator UG3OD035518 (Jennifer Straughen) tengfei.ma@hfhs.org
Emily S. Barrett   PhD Department of Biostatistics and Epidemiology Environmental and Occupational Health Sciences Institute, Rutgers University Piscataway, New Jersey, USA ECHO Cohort Study Site Principal Investigator UG3OD035527 (Emily S Barrett) emily.barrett@eoshi.rutgers.edu
Martin J. Blaser   MD Center for Advanced Biotechnology & Medicine Rutgers University Piscataway, New Jersey, USA ECHO Cohort Study Site Principal Investigator UG3OD035527 (Emily S Barrett) blaser@cabm.rutgers.edu
Maria Gloria Dominguez-Bello   PhD Departments of Biochemistry and Microbiology & Anthropology Rutgers University New Brunswick, New Jersey, USA ECHO Cohort Study Site Principal Investigator UG3OD035527 (Emily S Barrett) mg.dominguez-bello@rutgers.edu
Daniel B. Horton   MD Department of Pediatrics Robert Wood Johnson Medical School, Rutgers University New Brunswick, New Jersey, USA ECHO Cohort Study Site Principal Investigator UG3OD035527 (Emily S Barrett) daniel.horton@rutgers.edu
Manuel Jimenez   MD Departments of Pediatrics, Family Medicine, and Community Health Robert Wood Johnson Medical School, Rutgers University New Brunswick, New Jersey, USA ECHO Cohort Study Site Principal Investigator UG3OD035527 (Emily S Barrett) jimenema@rwjms.rutgers.edu
Todd Rosen   MD Department of Obstetrics, Gynecology, and Reproductive Sciences Robert Wood Johnson Medical School, Rutgers University New Brunswick, New Jersey, USA ECHO Cohort Study Site Co-Investigator UG3OD035527 (Emily S Barrett) rosentj@rwjms.rutgers.edu
Kristy Palomares   MD, PhD Department of Obstetrics and Gynecology Saint Peter's University Hospital New Brunswick, New Jersey, USA ECHO Cohort Study Site Co-Investigator UG3OD035527 (Emily S Barrett) kpalomares@saintpetersuh.com
Lyndsay A. Avalos   PhD, MPH Division of Research Kaiser Permanente Northern California Oakland, California, USA ECHO Cohort Study Site Principal Investigator UG3OD035540 (Monique Marie Hedderson) Lyndsay.A.Avalos@kp.org
Yeyi Zhu   PhD, MS Division of Research Kaiser Permanente Northern California Oakland, California, USA ECHO Cohort Study Site Principal Investigator UG3OD035540 (Monique Marie Hedderson) Yeyi.Zhu@kp.org
Kelly J . Hunt   PhD Department of Public Health Sciences Medical University of South Carolina Charleston, South Carolina, USA ECHO Cohort Study Site Principal Investigator UG3OD035543 (Kelly J Hunt) huntke@musc.edu
Roger B. Newman   MD Department of Obstetrics and Gynecology Medical University of South Carolina Charleston, South Carolina, USA ECHO Cohort Study Site Principal Investigator UG3OD035543 (Kelly J Hunt) newmanr@musc.edu
Michael S. Bloom   PhD Department of Global and Community Health George Mason University Fairfax, Virginia, USA ECHO Cohort Study Site Principal Investigator UG3OD035543 (Kelly J Hunt) mbloom22@gmu.edu
Mallory H. Alkis   MD Department of Obstetrics and Gynecology Medical University of South Carolina Charleston, South Carolina, USA ECHO Cohort Study Site Co-Investigator UG3OD035543 (Kelly J Hunt) hudsonm@musc.edu
James R. Roberts   MD, MPH Department of Pediatrics Medical University of South Carolina Charleston, South Carolina, USA ECHO Cohort Study Site Co-Investigator UG3OD035543 (Kelly J Hunt) robertsj@musc.edu
Sunni L. Mumford   PhD Department of Biostatistics, Epidemiology and Informatics; Department of Obstetrics and Gynecology University of Pennsylvania Perelman School of Medicine Philadelphia, Pennsylvania, USA ECHO Cohort Study Site Principal Investigator UG3OD035537 (Sunni L Mumford) sunni.mumford@pennmedicine.upenn.edu
Heather H. Burris   MD, MPH Division of Neonatology, Department of Pediatrics Children's Hospital of Philadelphia; University of Pennsylvania Perelman School of Medicine Philadelphia, Pennsylvania, USA ECHO Cohort Study Site Principal Investigator UG3OD035537 (Sunni L Mumford) BURRISH@chop.edu
Sara B. DeMauro   MD, MSCE Division of Neonatology, Department of Pediatrics Children's Hospital of Philadelphia; University of Pennsylvania Perelman School of Medicine Philadelphia, Pennsylvania, USA ECHO Cohort Study Site Principal Investigator UG3OD035537 (Sunni L Mumford) DEMAURO@chop.edu
Lynn M. Yee   MD, MPH Division of Maternal-Fetal Medicine, Department of Obstetrics & Gynecology Feinberg School of Medicine, Northwestern University Chicago, Illinois, USA ECHO Cohort Study Site Principal Investigator UG3OD035546 (Judy Aschner) lynn.yee@northwestern.edu
Aaron Hamvas   MD Division of Neonatology, Department of Pediatrics Ann & Robert H. Lurie Children's Hospital, Feinberg School of Medicine, Northwestern University Chicago, Illinois, USA ECHO Cohort Study Site Principal Investigator UG3OD035546 (Judy Aschner) ahamvas@luriechildrens.org
Antonia F. Olidipo   MD, MSCI Division of Maternal-Fetal Medicine, Department of Obstetrics & Gynecology Hackensack University Medical Center, Hackensack Meridian School of Medicine Nutley, New Jersey, USA ECHO Cohort Study Site Co-Investigator UG3OD035546 (Judy Aschner) antonia.olidipo@hmhn.org
Andrew S. Haddad   MD Division of Maternal-Fetal Medicine, Department of Obstetrics & Gynecology Hackensack University Medical Center, Hackensack Meridian School of Medicine Nutley, New Jersey, USA ECHO Cohort Study Site Co-Investigator UG3OD035546 (Judy Aschner) andrews.haddad@hmhn.org
Lisa R. Eiland   MD Division of Neonatology, Department of Pediatrics Hackensack University Medical Center, Hackensack Meridian School of Medicine Nutley, New Jersey, USA ECHO Cohort Study Site Co-Investigator UG3OD035546 (Judy Aschner) lisa.eiland@hmhn.org
Nicole T. Spillane   MD Division of Neonatology, Department of Pediatrics Hackensack University Medical Center, Hackensack Meridian School of Medicine Nutley, New Jersey, USA ECHO Cohort Study Site Co-Investigator UG3OD035546 (Judy Aschner) nicole.spillane@hmhn.org
Kirin N. Suri   MD Division of Developmental and Behavioral Pediatrics, Department of Pediatrics Hackensack University Medical Center, Hackensack Meridian School of Medicine Nutley, New Jersey, USA ECHO Cohort Study Site Co-Investigator UG3OD035546 (Judy Aschner) kirin.suri@hmhn.org
Stephanie A. Fisher   MD, MPH Division of Maternal-Fetal Medicine, Department of Obstetrics & Gynecology Feinberg School of Medicine, Northwestern University Chicago, Illinois, USA ECHO Cohort Study Site Co-Investigator UG3OD035546 (Judy Aschner) stephanie.fisher@northwestern.edu
Jeffrey A. Goldstein   MD, PhD Department of Pathology Feinberg School of Medicine, Northwestern University Chicago, Illinois, USA ECHO Cohort Study Site Co-Investigator UG3OD035546 (Judy Aschner) ja.goldstein@northwestern.edu
Leena B. Mithal   MD Division of Infectious Diseases, Department of Pediatrics Ann & Robert H. Lurie Children's Hospital, Feinberg School of Medicine, Northwestern University Chicago, Illinois, USA ECHO Cohort Study Site Co-Investigator UG3OD035546 (Judy Aschner) lmithal@luriechildrens.org
Raye-Ann O. DeRegnier   MD Division of Neonatology, Department of Pediatrics Ann & Robert H. Lurie Children's Hospital, Feinberg School of Medicine, Northwestern University Chicago, Illinois, USA ECHO Cohort Study Site Co-Investigator UG3OD035546 (Judy Aschner) r-deregnier@northwestern.edu
Nathalie L. Maitre   MD, PhD Division of Neonatology, Department of Pediatrics Emory University School of Medicine and Cerebral Palsy Foundation Atlanta, Georgia, USA and New York, New York, USA ECHO Cohort Study Site Co-Investigator UG3OD035546 (Judy Aschner) nathalie.linda.maitre@emory.edu
Ruby H.N. Nguyen   PhD, MHS Division of Epidemiology & Community Health School of Public Health, University of Minnesota Minneapolis, Minnesota, USA ECHO award Principal Investigator UG3OD035529 (Hong-Ngoc Nguyen) Nguyen@umn.edu
Meghan M. JaKa   PhD, MS Division of Research & Evaluation HealthPartners Institute Minneapolis, Minnesota, USA ECHO site Principal Investigator UG3OD035529 (Hong-Ngoc Nguyen) meghan.m.jaka@healthpartners.com
Abbey C. Sidebottom   PhD, MPH Care Delivery Research Allina Health Minneapolis, Minnesota, USA ECHO site Principal Investigator UG3OD035529 (Hong-Ngoc Nguyen) abbey.sidebottom@allina.com
Michael J. Paidas   MD Department of Obstetrics and Gynecology University of Miami Miller School of Medicine Miami, Florida, USA ECHO site Principal Investigator UG3OD035542 (Hudson Santos) mxp1440@med.miami.edu
JoNell E. Potter   APRN, PhD Department of Obstetrics, Gynecology and Reproductive Sciences University of Miami Miller School of Medicine Miami, Florida, USA ECHO Cohort Study Site Co-Investigator UG3OD035542 (Hudson Santos) jpotter2@med.miami.edu
Natale Ruby   PhD, PsyD Mailman Center for Child Development University of Miami Miller School of Medicine Miami, Florida, USA ECHO Cohort Study Site Co-Investigator UG3OD035542 (Hudson Santos) rnatale@med.miami.edu
Lunthita Duthely   EdD Department of Obstetrics, Gynecology and Reproductive Sciences and Department of Public Health Sciences University of Miami School of Medicine Miami, Florida, USA ECHO Cohort Study Site Co-Investigator UG3OD035542 (Hudson Santos) LDuthely@med.miami.edu
Arumugam Jayakumar   PhD Department of Obstetrics, Gynecology and Reproductive Sciences University of Miami Miller School of Medicine Miami, Florida, USA ECHO Cohort Study Site Co-Investigator UG3OD035542 (Hudson Santos) ajayakumar@med.miami.edu
Karen Young   MD Department of Pediatrics University of Miami Miller School of Medicine Miami, Florida, USA ECHO Cohort Study Site Co-Investigator UG3OD035542 (Hudson Santos) kyoung3@miami.edu
Isabel Maldonado   MPH, BS School of Nursing and Health Studies University of Miami Miami, Florida, USA ECHO Cohort Study Site Program Director UG3OD035542 (Hudson Santos) icm16@miami.edu
Meghan Miller   PhD Psychiatry and Behavioral Sciences; MIND Institute University of California Davis Sacramento, California, USA ECHO Cohort Study Site Co-Investigator UG3OD035550 (Rebecca Schmidt) mrhmiller@ucdavis.edu
Jonathan L. Slaughter   MD, MPH Center for Perinatal Research, Abigail Wexner Research Institute and Division of Neonatology, Nationwide Children's Hospital and Department of Pediatrics, College of Medicine and Division of Epidemiology, College of Public Health, The Ohio State University Nationwide Children's Hospital and The Ohio State University Columbus, Ohio, USA ECHO Cohort Study Site Principal Investigator UG3OD035536 (Jonathan Slaughter) jonathan.slaughter@nationwidechildrens.org
Sarah A. Keim   PhD, MS, MA Center for Biobehavioral Health, Abigail Wexner Research Institute, Nationwide Children's Hospital and Department of Pediatrics, College of Medicine and Division of Epidemiology, College of Public Health, The Ohio State University Nationwide Children's Hospital and The Ohio State University Columbus, Ohio, USA ECHO Cohort Study Site Principal Investigator UG3OD035536 (Jonathan Slaughter) Sarah.Keim@nationwidechildrens.org
Courtney D. Lynch   PhD, MPH Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, College of Medicine and Division of Epidemiology, College of Public Health, The Ohio State University The Ohio State University Columbus, Ohio, USA ECHO Cohort Study Site Principal Investigator UG3OD035536 (Jonathan Slaughter) Courtney.Lynch@osumc.edu
Kartik K. Venkatesh   MD, PhD Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, College of Medicine and Division of Epidemiology, College of Public Health, The Ohio State University The Ohio State University Columbus, Ohio, USA ECHO Cohort Study Site Principal Investigator UG3OD035536 (Jonathan Slaughter) kartik.venkatesh@osumc.edu
Kristina W. Whitworth   PhD Center for Precision Environmental Health and Department of Medicine Baylor College of Medicine Houston, Texas, USA ECHO Cohort Study Site Principal Investigator UG3OD035544 (Kristina Whitworth) kristina.whitworth@bcm.edu
Elaine Symanski   PhD Center for Precision Environmental Health and Department of Medicine Baylor College of Medicine Houston, Texas, USA ECHO Cohort Study Site Principal Investigator UG3OD035544 (Kristina Whitworth) elaine.symanski@bcm.edu
Thomas F. Northrup   PhD Department of Family and Community Medicine University of Texas Health Science Center at Houston (UTHealth Houston) McGovern Medical School Houston, Texas, USA ECHO Cohort Study Site Principal Investigator UG3OD035544 (Kristina Whitworth) thomas.f.northrup@uth.tmc.edu
Hector Mendez-Figueroa   MD Department of Obstetrics, Gynecology and Reproductive Sciences University of Texas Health Science Center at Houston (UTHealth Houston) McGovern Medical School Houston, Texas, USA ECHO Cohort Study Site Co-Investigator UG3OD035544 (Kristina Whitworth) hector.mendezfigueroa@uth.tmc.edu
Ricardo A. Mosquera   MD Department of Pediatrics University of Texas Health Science Center at Houston (UTHealth Houston) McGovern Medical School Houston, Texas, USA ECHO Cohort Study Site Co-Investigator UG3OD035544 (Kristina Whitworth) ricardo.a.mosquera@uth.tmc.edu
Margaret R. Karagas   PhD Department of Epidemiology Geisel School of Medicine at Dartmouth Hanover, New Hampshire, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023275 (Margaret Karagas) margaret.karagas@dartmouth.edu
Juliette C. Madan   MD, MS Departments of Psychiatry, Pediatrics & Epidemiology Geisel School of Medicine at Dartmouth, Dartmouth Hitchcock Medical Center Hanover, New Hampshire, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023275 (Margaret Karagas) juliette.madan@dartmouth.edu
Debra M. MacKenzie   PhD Community Environmental Health Program, Department of Pharmaceutical Sciences College of Pharmacy, University of New Mexico Health Sciences Center Albuquerque, New Mexico, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023344 (Debra MacKenzie) dmackenzie@salud.unm.edu
Johnnye L. Lewis   PhD Community Environmental Health Program, Department of Pharmaceutical Sciences College of Pharmacy, University of New Mexico Health Sciences Center Albuquerque, New Mexico, USA ECHO Cohort Study Site Principal Investigator UG3/UH3OD023344 (Debra MacKenzie) jlewis@cybermesa.com; jlewis@salud.unm.edu
Brandon J. Rennie   PhD Center for Development and Disability University of New Mexico Albuquerque, New Mexico, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023344 (Debra MacKenzie) Brennie@salud.unm.edu
Bennett L. Leventhal   MD Community Environmental Health Program, Department of Pharmaceutical Sciences UNM College of Pharmacy, University of New Mexico Health Sciences Center; University of Chicago Albuquerque, New Mexico, USA; Chicago, Illinois, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023344 (Debra MacKenzie) Bennett.leventhal@outlook.com
Young Shin Kim   MD, MS, MPH, PhD Department of Psychiatry and Behavioral Sciences University of California, San Francisco San Francisco, California, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023344 (Debra MacKenzie) Youngshin.Kim@ucsf.edu
Somer Bishop   PhD Department of Psychiatry and Behavioral Sciences University of California, San Francisco San Francisco, California, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023344 (Debra MacKenzie) Somer.Bishop@ucsf.com
Sara S. Nozadi   PhD Community Environmental Health Program, Department of Pharmaceutical Sciences College of Pharmacy, University of New Mexico Health Sciences Center Albuquerque, New Mexico, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023344 (Debra MacKenzie) snozadi@unm.edu
Li Luo   PhD Department of Internal Medicine Comprehensive Cancer Center, University of New Mexico Health Sciences Center Albuquerque, New Mexico, USA ECHO Cohort Study Site Co-Investigator UG3/UH3OD023344 (Debra MacKenzie) lluo@salud.unm.edu
Barry M. Lester   PhD Department of Pediatrics, Department of Psychiatry and Human Behavior Warren Alpert Medical School of Brown University Providence, Rhode Island, USA ECHO Cohort Study Site Principal Investigator UH3OD023347 (Barry Lester) barry_lester@brown.edu
Carmen J. Marsit   PhD Department of Environmental Health Rollins School of Public Health, Emory University Atlanta, Georgia, USA ECHO Cohort Study Site Principal Investigator UH3OD023347 (Barry Lester) carmen.j.marsit@emory.edu
Todd Everson   PhD Department of Environmental Health Rollins School of Public Health, Emory University Atlanta, Georgia, USA ECHO Cohort Study Site Principal Investigator UH3OD023347 (Barry Lester) todd.m.everson@emory.edu
Cynthia M. Loncar   PhD Department of Psychiatry and Human Behavior Warren Alpert Medical School of Brown University Providence, Rhode Island, USA ECHO Cohort Study Site Principal Investigator UH3OD023347 (Barry Lester) cloncar@kentri.org
Elisabeth C. McGowan   MD Department of Pediatrics Warren Alpert Medical School of Brown University Providence, Rhode Island, USA ECHO Cohort Study Site Principal Investigator UH3OD023347 (Barry Lester) emcgowan@wihri.org
Stephen J. Sheinkopf   PhD Department of Pediatrics Thompson Center for Autism & Neurodevelopment, University of Missouri Columbia, Missouri, USA ECHO Cohort Study Site Principal Investigator UH3OD023347 (Barry Lester) ssheinkopf@health.missouri.edu
Brian S. Carter   MD Department of Pediatrics Children's Mercy-Kansas City Kansas City, Missouri, USA ECHO Cohort Study Site Principal Investigator UH3OD023347 (Barry Lester) bscarter@cmh.edu
Jennifer Check   MD Department of Pediatrics Wake Forest School of Medicine Winston, Salem North Carolina, USA ECHO Cohort Study Site Principal Investigator UH3OD023347 (Barry Lester) jcheck@wakehealth.edu
Jennifer B. Helderman   MD Department of Pediatrics Wake Forest School of Medicine Winston, Salem North Carolina, USA ECHO Cohort Study Site Principal Investigator UH3OD023347 (Barry Lester) jhelderm@wakehealth.edu
Charles R. Neal   MD Department of Pediatrics University of Hawaii John A Burns School of Medicine Honolulu, Hawaii, USA ECHO Cohort Study Site Principal Investigator UH3OD023347 (Barry Lester) cneal@hphmg.org
Lynne M. Smith   MD Department of Pediatrics UCLA Clinical and Translational Science Institute at The Lundquist Institute, Harbor-UCLA Medical Center Los Angeles, California, USA ECHO Cohort Study Site Principal Investigator UH3OD023347 (Barry Lester) smith@lundquist.org-test

Contributor Information

Krystin Jones, Department of Epidemiology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, United States.

Bianca P Acevedo, Cohen Children’s Medical Center, Northwell Health, New Hyde Park, NY 11040, United States.

Lyndsay A Avalos, Kaiser Permanente Northern California, Division of Research, Pleasanton, CA 94588, United States.

Brennan H Baker, Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA 98105, United States; Seattle Children’s Research Institute, Seattle, WA 98101, United States.

Nicole R Bush, Department of Psychiatry and Behavioral Sciences, Department of Pediatrics, Weill Institute for Neurosciences, University of California, San Francisco, CA 94143,United States.

Claudia Buss, Charité—Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institute of Medical Psychology, Berlin 10117, Germany; Development, Health, and Disease Research Program and Department of Pediatrics, University of California Irvine, School of Medicine, Irvine, CA 92697, United States; German Center for Mental Health (DZPG), Partner Site Berlin, Charité—Universitätsmedizin, Berlin 10117, Germany; German Center for Child and Adolescent Health (DZKJ), Partner Site Berlin, Charité—Universitätsmedizin Berlin, Berlin 10117, Germany.

Luke P Grosvenor, Kaiser Permanente Northern California, Division of Research, Pleasanton, CA 94588, United States.

Alison E Hipwell, Department of Psychiatry, Psychology and Clinical & Translational Science, University of Pittsburgh, Pittsburgh, PA 15213, United States.

Kristine Marceau, Department of Human Development and Family Science, Purdue University, West Lafayette, IN 47906, United States.

Cindy T McEvoy, Department of Pediatrics, Papé Pediatric Research Institute, Oregon Health & Science University, Portland, OR 97239, United States.

Wei Perng, Department of Epidemiology, Colorado School of Public Health; Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, United States.

Alexandra D W Sullivan, Department of Psychiatry and Behavioral Sciences, Department of Pediatrics, Weill Institute for Neurosciences, University of California, San Francisco, CA 94143,United States.

Irene Tung, Department of Psychology, California State University, Dominguez Hills, Carson, CA 90747, United States.

Yeyi Zhu, Kaiser Permanente Northern California, Division of Research, Pleasanton, CA 94588, United States.

Christine Ladd-Acosta, Department of Epidemiology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, United States; Wendy Klag Center for Autism and Developmental Disabilities, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, United States.

Author contributions

Krystin Jones (Conceptualization [equal], Formal Analysis [equal], Visualization [lead], Writing – original draft [lead], Writing – review & editing [lead]), Bianca P. Acevedo (Writing – review & editing [supporting]), Lyndsay A. Avalos (Writing – review & editing [supporting]), Brennan H. Baker (Writing – review & editing [supporting]), Nicole R. Bush (Methodology [supporting], Writing – review & editing [supporting]), Claudia Buss (Writing – review & editing [equal]), Luke P. Grosvenor (Writing – review & editing [supporting]), Alison E. Hipwell (Writing – review & editing [supporting]), Kristine Marceau (Writing – review & editing [supporting]), Cindy T. McEvoy (Writing – review & editing [supporting]), Wei Perng (Writing – review & editing [supporting]), Alexandra D. W. Sullivan (Writing – review & editing [supporting]), Irene Tung (Writing – review & editing [supporting]), Yeyi Zhu (Writing – review & editing [supporting]), Christine Ladd-Acosta (Conceptualization [equal], Supervision [lead], Writing – original draft [supporting], Writing – review & editing [supporting])

Conflict of interest

Dr. Ladd-Acosta reports consulting fees from the University of Iowa for providing expertise on autism epigenetics, outside the scope of this work. All other co-authors declare no conflicts of interest.

Funding

Research reported in this publication was supported by the Environmental influences on Child Health Outcomes (ECHO) Program, Office of the Director, National Institutes of Health, under Award Numbers U2COD023375 (Coordinating Center), U24OD023382 (Data Analysis Center), U24OD023319 with co-funding from the Office of Behavioural and Social Science Research (Measurement Core), U24OD035523 (Lab Core), ES0266542 (HHEAR), U24ES026539 (HHEAR Barbara O'Brien), U2CES026533 (HHEAR Lisa Peterson), U2CES026542 (HHEAR Patrick Parsons, Kannan Kurunthacalam), U2CES030859 (HHEAR Manish Arora), U2CES030857 (HHEAR Timothy R. Fennell, Susan J. Sumner, Xiuxia Du), U2CES026555 (HHEAR Susan L. Teitelbaum), U2CES026561 (HHEAR Robert O. Wright), U2CES030851 (HHEAR Heather M. Stapleton, P. Lee Ferguson), UG3/UH3OD023251 (Akram Alshawabkeh), UH3OD023320 and UG3OD035546 (Judy Aschner), UH3OD023332 (Clancy Blair, Leonardo Trasande), UG3/UH3OD023253 (Carlos Camargo), UG3/UH3OD023248 and UG3OD035526 (Dana Dabelea), UG3/UH3OD023313 (Daphne Koinis Mitchell), UH3OD023328 (Cristiane Duarte), UH3OD023318 (Anne Dunlop), UG3/UH3OD023279 (Amy Elliott), UG3/UH3OD023289 (Assiamira Ferrara), UG3/UH3OD023282 (James Gern), UH3OD023287 (Carrie Breton), UG3/UH3OD023365 (Irva Hertz-Picciotto), UG3/UH3OD023244 (Alison Hipwell), UG3/UH3OD023275 (Margaret Karagas), UH3OD023271 and UG3OD035528 (Catherine Karr), UH3OD023347 (Barry Lester), UG3/UH3OD023389 (Leslie Leve), UG3/UH3OD023344 (Debra MacKenzie), UH3OD023268 (Scott Weiss), UG3/UH3OD023288 (Cynthia McEvoy), UG3/UH3OD023342 (Kristen Lyall), UG3/UH3OD023349 (Thomas O'Connor), UH3OD023286 and UG3OD035533 (Emily Oken), UG3/UH3OD023348 (Mike O'Shea), UG3/UH3OD023285 (Jean Kerver), UG3/UH3OD023290 (Julie Herbstman), UG3/UH3OD023272 (Susan Schantz), UG3/UH3OD023249 (Joseph Stanford), UG3/UH3OD023305 (Leonardo Trasande), UG3/UH3OD023337 (Rosalind Wright), UG3OD035508 (Sheela Sathyanarayana), UG3OD035509 (Anne Marie Singh), UG3OD035513 and UG3OD035532 (Annemarie Stroustrup), UG3OD035516 and UG3OD035517 (Tina Hartert), UG3OD035518 (Jennifer Straughen), UG3OD035519 (Qi Zhao), UG3OD035521 (Katherine Rivera-Spoljaric), UG3OD035527 (Emily S Barrett), UG3OD035540 (Monique Marie Hedderson), UG3OD035543 (Kelly J. Hunt), UG3OD035537 (Sunni L. Mumford), UG3OD035529 (Hong-Ngoc Nguyen), UG3OD035542 (Hudson Santos), UG3OD035550 (Rebecca Schmidt), UG3OD035536 (Jonathan Slaughter), and UG3OD035544 (Kristina Whitworth). The sponsor, NIH, participated in the overall design and implementation of the ECHO Program, which was funded as a cooperative agreement between NIH and grant awardees. The sponsor approved the Steering Committee-developed ECHO protocol and its amendments, including COVID-19 measures. The sponsor had no access to the central database, which was housed at the ECHO Data Analysis Center. Data management and site monitoring were performed by the ECHO Data Analysis Center and Coordinating Center. All analyses for scientific publication were performed by the study statistician, independently of the sponsor. The lead author wrote all drafts of the manuscript and made revisions based on co-authors and the ECHO Publication Committee (a subcommittee of the ECHO Operations Committee) feedback without input from the sponsor. The study sponsor did not review or approve the manuscript for submission to the journal.

Data availability

Select de-identified data from the ECHO Program are available through NICHD’s Data and Specimen Hub (DASH). Information on study data not available on DASH, such as some Indigenous datasets, can be found on the ECHO study DASH webpage.

References

  • 1. Burns  ER, Farr  SL, Howards  PP. Stressful life events experienced by women in the year before their infants’ births—United States, 2000–2010. MMWR Morb Mortal Wkly Rep. 2015;64:247–51. [PMC free article] [PubMed] [Google Scholar]
  • 2. Stressful life events experienced by women in the year before their infants’ births—United States, 2000–2010. https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6409a3.htm. (5 December, 2024, date last accessed).
  • 3. Woods  SM, Melville  JL, Guo  Y  et al.  Psychosocial stress during pregnancy. Am J Obstet Gynecol. 2010;202:61.e1–e7. 10.1016/j.ajog.2009.07.041 [DOI] [Google Scholar]
  • 4. Ronald  A, Pennell  CE, Whitehouse  AJO. Prenatal maternal stress associated with ADHD and autistic traits in early childhood. Front Psychol. 2010;1:223. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5. Grizenko  N.  Maternal stress during pregnancy, ADHD symptomatology in children and genotype: gene–environment interaction. J Can Acad Child Adolesc Psychiatry. 2012;21:9–15. [PMC free article] [PubMed] [Google Scholar]
  • 6. Class  QA, Abel  KM, Khashan  AS  et al.  Offspring psychopathology following preconception, prenatal and postnatal maternal bereavement stress. Psychol Med. 2014;44:71–84. 10.1017/S0033291713000780 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7. Van den Bergh  BRH, van den Heuvel  MI, Lahti  M, et al.  Prenatal developmental origins of behavior and mental health: the influence of maternal stress in pregnancy. Neurosci Biobehav Rev. 2020;117:26–64. [DOI] [PubMed] [Google Scholar]
  • 8. Wainstock  T, Anteby  E, Glasser  S  et al.  The association between prenatal maternal objective stress, perceived stress, preterm birth and low birthweight. J Matern Fetal Neonatal Med. 2013;26:973–77. 10.3109/14767058.2013.766696 [DOI] [PubMed] [Google Scholar]
  • 9. Azar  N, Booij  L. DNA methylation as a mediator in the association between prenatal maternal stress and child mental health outcomes: current state of knowledge. J Affect Disord. 2022;319:142–63. 10.1016/j.jad.2022.09.008 [DOI] [PubMed] [Google Scholar]
  • 10. Beijers  R, Buitelaar  JK, de Weerth  C. Mechanisms underlying the effects of prenatal psychosocial stress on child outcomes: beyond the HPA axis. Eur Child Adolesc Psychiatry. 2014;23:943–56. 10.1007/s00787-014-0566-3 [DOI] [PubMed] [Google Scholar]
  • 11. Cao-Lei  L. Prenatal stress and epigenetics. Neurosci Biobehav Rev. 2020;117:198–210. [DOI] [PubMed] [Google Scholar]
  • 12. Gibney  ER, Nolan  CM. Epigenetics and gene expression. Heredity. 2010;105:4–13. 10.1038/hdy.2010.54 [DOI] [PubMed] [Google Scholar]
  • 13. Peixoto  P, Cartron  P-F, Serandour  AA  et al.  From 1957 to nowadays: a brief history of epigenetics. Int J Mol Sci. 2020;21:7571. 10.3390/ijms21207571 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14. Holliday  R. Epigenetics: a historical overview. Epigenetics. 2006;1:76–80. 10.4161/epi.1.2.2762 [DOI] [PubMed] [Google Scholar]
  • 15. Kapoor  A, Petropoulos  S, Matthews  SG. Fetal programming of hypothalamic–pituitary–adrenal (HPA) axis function and behavior by synthetic glucocorticoids. Brain Res Rev. 2008;57:586–95. 10.1016/j.brainresrev.2007.06.013 [DOI] [PubMed] [Google Scholar]
  • 16. Sparrow  S, Manning  JR, Cartier  J  et al.  Epigenomic profiling of preterm infants reveals DNA methylation differences at sites associated with neural function. Transl Psychiatry. 2016;6:e716–16. 10.1038/tp.2015.210 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17. Menon  R, Conneely  KN, Smith  AK. DNA methylation: an epigenetic risk factor in preterm birth. Reprod Sci. 2012;19:6–13. 10.1177/1933719111424446 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18. Siu  MT, Weksberg  R. Epigenetics of autism spectrum disorder. Adv Exp Med Biol. 2017;978:63–90. [DOI] [PubMed] [Google Scholar]
  • 19. Davis  EP, Glynn  LM, Waffarn  F  et al.  Prenatal maternal stress programs infant stress regulation. J Child Psychol Psychiatry. 2011;52:119–29. 10.1111/j.1469-7610.2010.02314.x [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20. Tollenaar  MS, Beijers  R, Jansen  J  et al.  Maternal prenatal stress and cortisol reactivity to stressors in human infants. Stress. 2011;14:53–65. 10.3109/10253890.2010.499485 [DOI] [PubMed] [Google Scholar]
  • 21. Scassellati  C, Bonvicini  C, Faraone  SV  et al.  Biomarkers and attention-deficit/hyperactivity disorder: a systematic review and meta-analyses. J Am Acad Child Adolesc Psychiatry. 2012;51:1003–1019.e20. 10.1016/j.jaac.2012.08.015 [DOI] [PubMed] [Google Scholar]
  • 22. Zajkowska  Z, Gullett  N, Walsh  A  et al.  Cortisol and development of depression in adolescence and young adulthood—a systematic review and meta-analysis. Psychoneuroendocrinology. 2022;136:105625. 10.1016/j.psyneuen.2021.105625 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 23. Sosnowski  DW, Booth  C, York  TP  et al.  Maternal prenatal stress and infant DNA methylation: a systematic review. Dev Psychobiol. 2018;60:127–39. 10.1002/dev.21604 [DOI] [PubMed] [Google Scholar]
  • 24. Hompes  T, Izzi  B, Gellens  E  et al.  Investigating the influence of maternal cortisol and emotional state during pregnancy on the DNA methylation status of the glucocorticoid receptor gene (NR3C1) promoter region in cord blood. J Psychiatr Res. 2013;47:880–91. 10.1016/j.jpsychires.2013.03.009 [DOI] [PubMed] [Google Scholar]
  • 25. Oberlander  TF, Weinberg  J, Papsdorf  M  et al.  Prenatal exposure to maternal depression, neonatal methylation of human glucocorticoid receptor gene (NR3C1) and infant cortisol stress responses. Epigenetics. 2008;3:97–106. 10.4161/epi.3.2.6034 [DOI] [PubMed] [Google Scholar]
  • 26. Ostlund  BD, Conradt  E, Crowell  SE  et al.  Prenatal stress, fearfulness, and the epigenome: exploratory analysis of sex differences in DNA methylation of the glucocorticoid receptor gene. Front Behav Neurosci. 2016;10:147. 10.3389/fnbeh.2016.00147 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27. Mansell  T, Vuillermin  P, Ponsonby  A-L  et al.  Maternal mental well-being during pregnancy and glucocorticoid receptor gene promoter methylation in the neonate. Dev Psychopathol. 2016;28:1421–30. 10.1017/S0954579416000183 [DOI] [PubMed] [Google Scholar]
  • 28. Braithwaite  EC, Kundakovic  M, Ramchandani  PG  et al.  Maternal prenatal depressive symptoms predict infant NR3C1 1F and BDNF IV DNA methylation. Epigenetics. 2015;10:408–17. 10.1080/15592294.2015.1039221 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 29. PubChem . HSD11B2–hydroxysteroid 11-beta dehydrogenase 2 (human). 2023. https://pubchem.ncbi.nlm.nih.gov/gene/HSD11B2/human. (5 December 2024, date last acessed).
  • 30. FKBP5 FKBP prolyl isomerase 5 [Homo sapiens (human)]—Gene—NCBI. https://www.ncbi.nlm.nih.gov/gene/2289. (5 December 2024, date last accessed).
  • 31. Monk  C, Feng  T, Lee  S  et al.  Distress during pregnancy: epigenetic regulation of placenta glucocorticoid-related genes and fetal neurobehavior. Am J Psychiatry. 2016;173:705–13. 10.1176/appi.ajp.2015.15091171 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 32. Kertes  DA, Kamin  HS, Hughes  DA  et al.  Prenatal maternal stress predicts methylation of genes regulating the hypothalamic-pituitary-adrenocortical system in mothers and newborns in the democratic republic of congo. Child Dev. 2016;87:61. 10.1111/cdev.12487 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 33. Conradt  E, Lester  BM, Appleton  AA  et al.  The roles of DNA methylation of NR3C1 and 11β-HSD2 and exposure to maternal mood disorder in utero on newborn neurobehavior. Epigenetics. 2013;8:1321–29. 10.4161/epi.26634 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 34. Marsit  CJ. Influence of environmental exposure on human epigenetic regulation. J Exp Biol. 2015;218:71–79. 10.1242/jeb.106971 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 35. Perroud  N, Rutembesa  E, Paoloni-Giacobino  A  et al.  The Tutsi genocide and transgenerational transmission of maternal stress: epigenetics and biology of the HPA axis. World J Biol Psychiatry. 2014;15:334–45. 10.3109/15622975.2013.866693 [DOI] [PubMed] [Google Scholar]
  • 36. Epel  ES, Crosswell  AD, Mayer  SE  et al.  More than a feeling: a unified view of stress measurement for population science. Front Neuroendocrinol. 2018;49:146–69. 10.1016/j.yfrne.2018.03.001 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 37. Cohen  S, Gianaros  PJ, Manuck  SB. A stage model of stress and disease. Perspect Psychol Sci. 2016;11:456–63. 10.1177/1745691616646305 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 38. Cohen  S, Kamarck  T, Mermelstein  R. A global measure of perceived stress. J Health Soc Behav. 1983;24:385–96. 10.2307/2136404 [DOI] [PubMed] [Google Scholar]
  • 39. Wu  MC, Lee  S, Cai  T  et al.  Rare-variant association testing for sequencing data with the sequence kernel association test. Am Hum Genet. 2011;89:82–93. 10.1016/j.ajhg.2011.05.029 [DOI] [Google Scholar]
  • 40. Wang  B, DeStefano  AL, Lin  H. Integrative methylation score to identify epigenetic modifications associated with lipid changes resulting from fenofibrate treatment in families. BMC Proc. 2018;12:28. 10.1186/s12919-018-0125-x [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 41. Fuady  AM, Lent  S, Sarnowski  C  et al.  Application of novel and existing methods to identify genes with evidence of epigenetic association: results from GAW20. BMC Genet. 2018;19:72. 10.1186/s12863-018-0647-2 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 42. Knapp  EA, Kress  AM, Parker  CB  et al.  The Environmental Influences on Child Health Outcomes (ECHO)-wide cohort. Am J Epidemiol. 2023;192:1249–63. 10.1093/aje/kwad071 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 43. Blaisdell  CJ, Park  C, Hanspal  M  et al.  The NIH ECHO Program: investigating how early environmental influences affect child health. Pediatr Res. 2022;92:1215. 10.1038/s41390-021-01574-8 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 44. Park  CH, Blaisdell  CJ, Arteaga  SS  et al.  How the Environmental Influences on Child Health Outcome (ECHO) cohort can spur discoveries in environmental epidemiology. Am J Epidemiol. 2024;193:1219–23. 10.1093/aje/kwae073 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 45. Cohen  S, Wiliamson  G. Perceived stress in a probability sample of the United States. In: Spacapam  S, Oskamp  S (eds.), The Social Psychology of Health: Claremont Symposium on Applied Social Psychology. Newbury Park, CA: Sage Publications, 1988. [Google Scholar]
  • 46. Reise  SP, Moore  TM. Item response theory. In: Cooper  H, Coutanche  MN, McMullen  LMet al. APA Handbook of Research Methods in Psychology: Foundations, Planning, Measures, and Psychometrics, Vol. 1, 2nd ed.  Washington, DC: American Psychological Association, 2023, 809–35. 10.1037/0000318-037 [DOI] [Google Scholar]
  • 47. Slotkin  J. NIH Toolbox Scoring and Interpretation Guide. 2012.
  • 48. Ladd-Acosta  C, Vang  E, Barrett  ES  et al.  Analysis of pregnancy complications and epigenetic gestational age of newborns. JAMA Netw Open. 2023;6:e230672. 10.1001/jamanetworkopen.2023.0672 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 49. Pilkonis  PA, Choi  SW, Reise  SP  et al.  Item banks for measuring emotional distress from the patient-reported outcomes measurement information system (PROMIS®): depression, anxiety, and anger. Assessment. 2011;18:263–83. 10.1177/1073191111411667 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 50. Blackwell  CK, Wakschlag  LS, Gershon  RC  et al.  Measurement framework for the Environmental Influences on Child Health Outcomes research program. Curr Opin Pediatr. 2018;30:276–84. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 51. R Core Team . R: A Language and Environment for Statistical Computing. Vienna, Austria: R Foundation for Statistical Computing, 2024. [Google Scholar]
  • 52. Stekhoven  DJ, Bühlmann  P. MissForest—non-parametric missing value imputation for mixed-type data. Bioinformatics. 2012;28:112–18. 10.1093/bioinformatics/btr597 [DOI] [PubMed] [Google Scholar]
  • 53. Leek  JT, Johnson  WE, Parker  HS  et al.  The sva package for removing batch effects and other unwanted variation in high-throughput experiments. Bioinformatics. 2012;28:882. 10.1093/bioinformatics/bts034 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 54. Ritchie  ME, Phipson  B, Wu  D  et al.  limma powers differential expression analyses for RNA-sequencing and microarray studies. Nucleic Acids Res. 2015;43:e47. 10.1093/nar/gkv007 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 55. Willer  CJ, Li  Y, Abecasis  GR. METAL: fast and efficient meta-analysis of genomewide association scans. Bioinformatics. 2010;26:2190–91. 10.1093/bioinformatics/btq340 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 56. Lee  S, Wu  MC, Lin  X. Optimal tests for rare variant effects in sequencing association studies. Biostatistics. 2012;13:762. 10.1093/biostatistics/kxs014 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 57. Holdsworth  EA, Schell  LM, Appleton  AA. Maternal–infant interaction quality is associated with child NR3C1 CpG site methylation at 7 years of age. Am J Hum Biol. 2023;35:e23876. 10.1002/ajhb.23876 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 58. Murgatroyd  C, Quinn  JP, Sharp  HM  et al.  Effects of prenatal and postnatal depression, and maternal stroking, at the glucocorticoid receptor gene. Translational Psychiatry. 2015;5:e560. 10.1038/tp.2014.140 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 59. Pedersen  BS, Schwartz  DA, Yang  IV  et al.  Comb-p: software for combining, analyzing, grouping and correcting spatially correlated P-values. Bioinformatics. 2012;28:2986–88. 10.1093/bioinformatics/bts545 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 60. Moore  LD, Le  T, Fan  G. DNA methylation and its basic function. Neuropsychopharmacology. 2013;38:23–38. 10.1038/npp.2012.112 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 61. Appleton  AA, Armstrong  DA, Lesseur  C  et al.  Patterning in placental 11-B hydroxysteroid dehydrogenase methylation according to prenatal socioeconomic adversity. PLoS One. 2013;8:e74691. 10.1371/journal.pone.0074691 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 62. Sutherland  S, Brunwasser  SM. Sex differences in vulnerability to prenatal stress: a review of the recent literature. Curr Psychiatry Rep. 2018;20:102. 10.1007/s11920-018-0961-4 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 63. Bronson  SL, Bale  TL. The placenta as a mediator of stress effects on neurodevelopmental reprogramming. Neuropsychopharmacology. 2016;41:207. 10.1038/npp.2015.231 [DOI] [PMC free article] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

dvaf024_Supplemental_File

Data Availability Statement

Select de-identified data from the ECHO Program are available through NICHD’s Data and Specimen Hub (DASH). Information on study data not available on DASH, such as some Indigenous datasets, can be found on the ECHO study DASH webpage.


Articles from Environmental Epigenetics are provided here courtesy of Oxford University Press

RESOURCES