Background

Residential proximity to major roadways, and prenatal exposures to particulate matter <2.5 μm (PM_2.5) and ozone (O₃) are linked to poor fetal outcomes but their relationship with childhood development is unclear.

Objectives

We investigated whether proximity to major roadways, or prenatal and early-life exposures to PM_2.5 and O₃ increase the risk of early developmental delays.

Study design

Prospective cohort.

Settings

New York State excluding New York City.

Participants

4089 singletons and 1016 twins born between 2008 and 2010.

Exposures

Proximity to major roadway was calculated using road network data from the NY Department of Transportation. Concentrations of PM_2.5 and O₃ estimated by the Environmental Protection Agency Downscaler models were spatiotemporally linked to each child's prenatal and early-life addresses incorporating residential history, and locations of maternal work and day-care.

Outcomes

Parents reported their children's development at ages 8, 12, 18, 24, 30 and 36 months in five domains using the Ages and Stages Questionnaire. Generalized mixed models estimated the relative risk (RR) and 95% CI for failing any developmental domain per 10 units increase in PM_2.5 and O₃, and for those living <1000 m away from a major roadway compared to those living further. Models adjusted for potential confounders.

Results

Compared to those >1000 m away from a major roadway, those resided 50-100 m [RR: 2.12 (1.00-4.52)] and 100-500 m [RR: 2.07 (1.02-4.22)] away had twice the risk of failing the communication domain. Prenatal exposures to both PM_2.5 and ozone during various pregnancy windows had weak but significant associations with failing any developmental domain with effects ranging from 1.6% to 2.7% for a 10 μg/m³ increase in PM_2.5 and 0.7%-1.7% for a 10 ppb increase in ozone. Average daily postnatal ozone exposure was positively associated with failing the overall screening by 8 months [3.3% (1.1%-5.5%)], 12 months [17.7% (10.4%-25.5%)], and 30 months [7.6%, (1.3%-14.3%)]. Findings were mixed for postnatal PM_2.5 exposures.

Conclusions

In this prospective cohort study, proximity to major roadway and prenatal/early-life exposures to PM_2.5 and O₃ were associated with developmental delays. While awaiting larger studies with personal air pollution assessment, efforts to minimize air pollution exposures during critical developmental windows may be warranted.

Objective

Examine the association of prepregnancy habitual consumption of fruits and fruit juices and gestational diabetes mellitus (GDM) risk.

Research design and methods

A prospective study among women with at least one singleton pregnancy in the Nurses' Health Study II from 1991 to 2001.

Results

Among 13,475 women, 860 reported a first diagnosis of GDM. The adjusted relative risks (RRs) for GDM from the lowest to highest quintile of whole fruit consumption were 1.00 (referent), 0.80 (95% CI 0.65-0.98), 0.90 (0.73-1.10), 0.80 (0.64-1.00), and 0.93 (0.76-1.16), respectively. The corresponding RRs for fruit juice were 1.00, 0.82 (0.66-1.01), 0.78 (0.63-0.96), 0.84 (0.68-1.04), and 1.00 (0.81-1.23).

Conclusions

These data suggest that prepregnancy higher consumption of whole fruits is not associated with an increased GDM risk. The association between fruit juices and GDM risk appears to be nonlinear.

Background

Obese women are less likely to initiate and continue breastfeeding. We described barriers to breastfeeding and examined the association between support from a health professional and breastfeeding knowledge and practices, by prepregnancy obesity status.

Methods

Using data from the Infant Feeding Practices Study II, a cohort of U.S. women (N = 2,997), we performed descriptive statistics to describe barriers to breastfeeding by prepregnancy obesity status. We conducted multivariable regression to examine the association of breastfeeding support from a physician or nonphysician health professional with knowledge of the recommended duration of breastfeeding, breastfeeding initiation, and breastfeeding duration, and whether breastfeeding support had different associations with outcomes by prepregnancy obesity status. Average marginal effects were calculated from regression models to interpret results as percentage-point changes.

Findings

Believing that formula was as good as breast milk was the most commonly cited reason for not initiating breastfeeding, and milk supply concerns were cited as reasons for not continuing breastfeeding. Physician breastfeeding support was associated with a 9.4 percentage-point increase (p < .05) in breastfeeding knowledge among obese women, although no increase was observed among nonobese women. Breastfeeding support from a physician or nonphysician health professional was associated with a significantly increased probability of breastfeeding initiation (8.5 and 12.5 percentage points, respectively) and breastfeeding for 6 months (12.5 and 8.4 percentage points, respectively), without differential associations by prepregnancy obesity.

Conclusions

Support for exclusive breastfeeding is an important predictor of breastfeeding initiation and duration among obese and nonobese women. Health educational interventions tailored to obese women might improve their breastfeeding initiation and continuation.

Objective

Consumption of sugar-sweetened beverages (SSBs) was related to an elevated risk of type 2 diabetes and insulin resistance in several recent studies among middle- or older-aged populations. Studies on SSB consumption and glucose intolerance among pregnant women, however, are lacking. We therefore examined the association between regular SSB consumption before pregnancy and the risk of gestational diabetes mellitus (GDM).

Research design and methods

This was a prospective study among 13,475 U.S. women who reported at least one singleton pregnancy between 1992 and 2001 in the Nurses' Health Study II. GDM was self-reported and validated by medical record review in a subsample. Cox proportional hazards models with multivariate adjustments were applied to examine the association of SSB consumption with GDM risk.

Results

During 10 years of follow-up, 860 incident GDM case subjects were identified. After adjustment for age, parity, race, physical activity, smoking, alcohol intake, prepregnancy BMI, and Western dietary pattern, intake of sugar-sweetened cola was positively associated with the risk of GDM, whereas no significant association was found for other SSBs and diet beverages. Compared with women who consumed <1 serving/month, those who consumed >or=5 servings/week of sugar-sweetened cola had a 22% greater GDM risk (relative risk 1.22 [95% CI 1.01-1.47]).

Conclusions

Findings from this study suggest that prepregnancy higher consumption of sugar-sweetened cola (>or=5 servings/week) is associated with an elevated GDM risk, whereas no significant association with GDM risk was observed for other SSBs and diet beverages.

Objective

To examine the association between age at menarche and risk of gestational diabetes mellitus (GDM).

Research design and methods

A prospective cohort study of 42,109 eligible pregnancies from 27,482 women in the Nurses' Health Study II.

Results

The adjusted risk ratios for GDM across the age at menarche categories (≤11, 12, 13, and ≥14 years) were 1.34 (95% CI 1.14-1.58), 1.13 (0.97-1.31), 1.11 (0.95-1.29), and 1.00 (referent; P for trend = 0.0005), respectively. Analysis of the mediating effect indicated that 42.1% (P = 0.0007) of the association was mediated through prepregnancy BMI.

Conclusions

These findings suggested that earlier menarche was significantly associated with an increased risk of GDM. This association was largely mediated through prepregnancy excessive body adiposity.

Worldwide trends to delay childbearing have increased parental ages at birth. Older parental age may harm offspring health, but mechanisms remain unclear. Alterations in offspring DNA methylation (DNAm) patterns could play a role as aging has been associated with methylation changes in gametes of older individuals. We meta-analyzed epigenome-wide associations of parental age with offspring blood DNAm of over 9500 newborns and 2000 children (5-10 years old) from the Pregnancy and Childhood Epigenetics consortium. In newborns, we identified 33 CpG sites in 13 loci with DNAm associated with maternal age (P_FDR < 0.05). Eight of these CpGs were located near/in the MTNR1B gene, coding for a melatonin receptor. Regional analysis identified them together as a differentially methylated region consisting of 9 CpGs in/near MTNR1B, at which higher DNAm was associated with greater maternal age (P_FDR = 6.92 × 10^-8) in newborns. In childhood blood samples, these differences in blood DNAm of MTNR1B CpGs were nominally significant (p < 0.05) and retained the same positive direction, suggesting persistence of associations. Maternal age was also positively associated with higher DNA methylation at three CpGs in RTEL1-TNFRSF6B at birth (P_FDR < 0.05) and nominally in childhood (p < 0.0001). Of the remaining 10 CpGs also persistent in childhood, methylation at cg26709300 in YPEL3/BOLA2B in external data was associated with expression of ITGAL, an immune regulator. While further study is needed to establish causality, particularly due to the small effect sizes observed, our results potentially support offspring DNAm as a mechanism underlying associations of maternal age with child health.

BACKGROUND: Seasonal variations in environmental exposures at birth or during gestation are associated with numerous adult traits and health outcomes later in life. Whether DNA methylation (DNAm) plays a role in the molecular mechanisms underlying the associations between birth season and lifelong phenotypes remains unclear. METHODS: We carried out epigenome-wide meta-analyses within the Pregnancy And Childhood Epigenetic Consortium to identify associations of DNAm with birth season, both at differentially methylated probes (DMPs) and regions (DMRs). Associations were examined at two time points: at birth (21 cohorts, N = 9358) and in children aged 1-11 years (12 cohorts, N = 3610). We conducted meta-analyses to assess the impact of latitude on birth season-specific associations at both time points. RESULTS: We identified associations between birth season and DNAm (False Discovery Rate-adjusted p values < 0.05) at two CpGs at birth (winter-born) and four in the childhood (summer-born) analyses when compared to children born in autumn. Furthermore, we identified twenty-six differentially methylated regions (DMR) at birth (winter-born: 8, spring-born: 15, summer-born: 3) and thirty-two in childhood (winter-born: 12, spring and summer: 10 each) meta-analyses with few overlapping DMRs between the birth seasons or the two time points. The DMRs were associated with genes of known functions in tumorigenesis, psychiatric/neurological disorders, inflammation, or immunity, amongst others. Latitude-stratified meta-analyses [higher (≥ 50°N), lower (< 50°N, northern hemisphere only)] revealed differences in associations between birth season and DNAm by birth latitude. DMR analysis implicated genes with previously reported links to schizophrenia (LAX1), skin disorders (PSORS1C, LTB4R), and airway inflammation including asthma (LTB4R), present only at birth in the higher latitudes (≥ 50°N). CONCLUSIONS: In this large epigenome-wide meta-analysis study, we provide evidence for (i) associations between DNAm and season of birth that are unique for the seasons of the year (temporal effect) and (ii) latitude-dependent variations in the seasonal associations (spatial effect). DNAm could play a role in the molecular mechanisms underlying the effect of birth season on adult health outcomes.

Maternal educational attainment (MEA) shapes offspring health through multiple potential pathways. Differential DNA methylation may provide a mechanistic understanding of these long-term associations. We aimed to quantify the associations of MEA with offspring DNA methylation levels at birth, in childhood and in adolescence. Using 37 studies from high-income countries, we performed meta-analysis of epigenome-wide association studies (EWAS) to quantify the associations of completed years of MEA at the time of pregnancy with offspring DNA methylation levels at birth (n = 9 881), in childhood (n = 2 017), and adolescence (n = 2 740), adjusting for relevant covariates. MEA was found to be associated with DNA methylation at 473 cytosine-phosphate-guanine sites at birth, one in childhood, and four in adolescence. We observed enrichment for findings from previous EWAS on maternal folate, vitamin-B₁₂ concentrations, maternal smoking, and pre-pregnancy BMI. The associations were directionally consistent with MEA being inversely associated with behaviours including smoking and BMI. Our findings form a bridge between socio-economic factors and biology and highlight potential pathways underlying effects of maternal education. The results broaden our understanding of bio-social associations linked to differential DNA methylation in multiple early stages of life. The data generated also offers an important resource to help a more precise understanding of the social determinants of health.