Association between parent's Body Mass Index (BMI) and their children, has been widely documented. Individual, familiar and structural factors play a role in this relation. We analyzed the ...association between maternal BMI change during the first year post-partum and their offspring's growth-trajectories and energy intake in their first five years of life.
Compare growth-trajectories and children's caloric intake according to post-partum mother´s BMI classification.
The anthropometric assessment was taken in 935 mother-child pairs along the study period. Mothers were classified into four groups according to their BMI-trajectories in the post-partum. Children's weight for height z-scores (WHZ) was compared among groups using random-effects regression models. A longitudinal comparison of children's caloric intake by the maternal group was carried out.
At 42 months of age, infants from mothers that remained overweight during the first year post-partum had, on average, 0.61 SD higher WHZ than those from mothers who remained in a recommended BMI group (R-BMI) in the same period. At 60 months of age, children´s prevalence of obesity was almost twice in the maternal overweight group vs R-BMI group (14.2% and 7.3% respectively). Chances for a child of having an over caloric intake were 36.5% (95% IC: 6.6%, 74.8%) and significantly higher among children from overweight mothers than those from R-BMI mothers. The difference in children's WHZ trajectory remained significant after adjusting for caloric intake, suggesting that contextual factors play a role in shaping children's obesity. A concurrent ethnographic study with the study subjects provides suggestions as to what these factors might be, including changes in the food landscape.
Children from overweight mothers tended to have a more caloric diet yielding a higher propensity to obesity. Contextual factors such as food landscape might contribute to childhood obesity beyond having an overweight mother. Pregnancy and post-partum is a window of opportunity for interventions to decrease the incidence of children's overweight.
Objective
The aim of this study was to evaluate whether short sleep duration or later sleep timing is a risk factor for insulin resistance (IR) in late adolescence.
Methods
Mexico City adolescents ...enrolled in a longitudinal birth cohort (ELEMENT) took part in two study visits during peri‐puberty that occurred approximately 2 years apart. IR was assessed with serum glucose and insulin. Four groups were defined using puberty‐specific cut points: no IR over the follow‐up period, transition from normal to IR, transition from IR to normal, and IR at both time points. Baseline sleep assessments were measured with 7‐day wrist actigraphy. Multinomial logistic regression models were used to evaluate associations between sleep duration and timing with homeostatic model assessment of insulin resistance categories, adjusting for age, sex, and baseline pubertal status.
Results
Adolescents who were ≥ 1 hour below the sleep duration recommendations‐for‐age were 2.74 times more likely to develop IR (95% CI: 1.0‐7.4). Similarly, adolescents who were in the latest category of sleep midpoint (>4:33 a.m.) were more likely than those with earliest midpoints (1 a.m.–3 a.m.) to develop IR (odds ratio = 2.63, 95% CI: 1.0‐6.7). Changes in adiposity over follow‐up did not mediate sleep and IR.
Conclusions
Insufficient sleep duration and late sleep timing were associated with development of IR over a 2‐year period in late adolescence.
•Exposure biomarkers were measured in urine collected during pregnancy and boyhood.•Some prenatal exposures were associated with reduced odds of adrenarche and puberty.•Prenatal exposures were not ...associated with boyhood hormone levels.•Boyhood exposures were not associated with adrenarche or puberty.•Some boyhood exposures were associated with decreased testosterone levels.
Phthalates and BPA are known endocrine disruptors and exposure in pregnant mothers and children is ubiquitous. We explored the relationship of prenatal and childhood exposures with pubertal onset and sex hormones in boys (ages 8–14). Phthalate metabolites and BPA were measured in maternal 3rd trimester or childhood urine. Sex hormones DHEAS, estradiol, inhibin B, SHBG, and total testosterone were measured in serum. Adrenarche and puberty were assessed by pediatrician. Prenatal exposure to some phthalates was associated with decreased DHEAS and inhibin B levels, and with increased SHBG. Prenatal exposure to most phthalates and BPA was associated with greatly reduced odds of adrenarche (odds ratios OR=0.12–0.65) and slightly reduced odds of puberty (OR=0.50–0.98). Childhood exposure was not associated with adrenarche or puberty, but some phthalates and BPA were associated with increased SHBG levels and decreased total and free testosterone levels.
Phthalates are associated with several adverse health outcomes, but few studies have evaluated phthalate exposures in Mexican populations, particularly pregnant women. Between 2007 and 2011, 948 ...pregnant women from Mexico City were recruited as part of the PROGRESS cohort. We quantified 17 metabolites of phthalates and phthalate alternatives in urine samples collected during the second and third trimesters and examined temporal trends of metabolite concentrations, within-person reproducibility, and relations of individual metabolites with sociodemographic, lifestyle, and occupational factors. Concentrations of mono-2-ethyl-5-carboxypentyl terephthalate, a metabolite of the alternative phthalate di-2-ethylhexyl terephthalate, increased monotonically from 2007 to 2010 (31% per year; 95% confidence interval = 23 and 39%). We observed moderate to high correlations among metabolites collected at the same visit, but there was high variability between second and third trimester phthalate metabolite concentrations (intraclass correlation coefficients = 0.17–0.35). In general, higher socioeconomic status was associated with higher phthalate concentrations. Some metabolites were associated with maternal age and education, but no consistent patterns were observed. Women working in the home and those who worked in administration had higher concentrations of several phthalate metabolites relative to students, professionals, and those in customer service. Biomonitoring efforts are warranted to investigate present and future exposure trends and patterns.
Previous studies suggest that prenatal phthalate exposure affects neurodevelopment and behavior during the first years of life.
To evaluate the effect of maternal urinary concentrations of phthalate ...metabolites during pregnancy on mental and psychomotor development in children 24–36months of age.
This analysis was conducted on the first three years of life among a subsample of 136 mother–child pairs from the ELEMENT cohort studies conducted in Mexico City. Maternal urine samples collected during the third trimester of pregnancy were analyzed for 9 phthalate metabolites: Mono-ethyl phthalate (MEP), Mono-n-butyl phthalate (MnBP), mono-isobutyl phthalate (MiBP), mono-benzyl phthalate (MBzP), Mono-3-carboxypropyl phthalate (MCPP), and four di-2-ethylhexyl phthalate (DEHP) metabolites mono-2-ethylhexyl-phthalate (MEHP), mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP). Among the 136 children, 135 (99.3%) completed the study period. Child neurodevelopment was assessed using mental and psychomotor development indexes (MDI and PDI) from a Bayley (BSID II) test at 24, 30, and 36months of age. The effect of prenatal phthalate exposure on neurodevelopment was estimated using linear regression models for longitudinal data clustered at the individual level.
No significant associations were observed among all children combined, but differential effects by gender were found. Among girls, there was a negative association between MDI and DEHP metabolites MEHP (β=−2.11 95% CI: −3.73, −0.49), MEHHP (β=−1.89 95% CI: −3.64, −0.15), MEOHP (β=−1.80 95% CI: −3.58, −0.03) MECPP (β=−2.52 95% CI: −4.44, −0.61), and ΣDEHP (β=−3.41 95% CI: −5.26, −1.55); there was no significant effect among boys. Male PDI was positively related to MBzP (β=1.79 95% CI: 0.14, 3.45) and MCPP (β=1.64 95% CI: 0.15, 3.12); there was no significant effect on PDI among girls.
This study demonstrates that sex plays a role of an effect modifier in the association between prenatal phthalate exposure and neurodevelopment.
•In a cohort study, a differential effect of prenatal phthalate exposure by gender was found.•A negative effect among girls between MDI and HMWP was estimated.•There was no effect between MDI and phthalates among boys.•A positive effect between prenatal LMWP exposure and PDI was estimated for boys.
Gestational lead (Pb) exposure can adversely affect offspring health through multiple mechanisms, including epigenomic alterations via DNA methylation (5mC) and hydroxymethylation (5hmC), an ...intermediate in oxidative demethylation. Most current methods do not distinguish between 5mC and 5hmC, limiting insights into their individual roles.
Our study sought to identify the association of trimester-specific (T1, T2, T3) prenatal Pb exposure with 5mC and 5hmC levels at multiple cytosine-phosphate-guanine sites within gene regions previously associated with prenatal Pb (
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,
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in whole blood leukocytes of children ages 11-18 years of age.
Participants from the Early Life Exposure in Mexico to Environmental Toxicants (ELEMENT) birth cohorts were selected (
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) and 5mC only; 5hmC is estimated by subtraction.
Participants were 51% male, and mean maternal blood lead levels (BLL) were
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5mC was negatively correlated with gene expression (Pearson
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These findings suggest there is variable 5hmC in human whole blood and that prenatal Pb exposure is associated with gene-specific 5mC and 5hmC levels at adolescence, providing evidence to consider 5hmC as a regulatory mechanism that is responsive to environmental exposures. https://doi.org/10.1289/EHP8507.
Prenatal phthalates exposures have been related to adiposity in peripuberty in a sex-specific fashion. Untargeted metabolomics analysis to assess circulating metabolites offers the potential to ...characterize biochemical pathways by which early life exposures influence the development of cardiometabolic risk during childhood and adolescence, prior to becoming evident in clinical markers.
Among mother-child dyads from the Early Life Exposure in Mexico to ENvironmental Toxicants (ELEMENT) birth cohort, we measured 9 phthalate metabolites and bisphenol A in maternal spot urine samples obtained during each trimester of pregnancy, corrected for urinary specific gravity and natural log-transformed. In 110 boys and 124 girls aged 8-14 years, we used a mass-spectrometry based untargeted metabolomics platform to measure fasting serum metabolites, yielding 572 annotated metabolites. We estimated the associations between trimester-specific urinary toxicants and each serum metabolite, among all children or stratified by sex and adjusting for child age, BMI z-score, and pubertal onset. We accounted for multiple comparisons using a 10% false discovery rate (q<0.1).
Associations between exposures and metabolites were observed among all children and in sex-stratified analyses (q<0.1). First trimester MEP, MiBP, and MCPP were associated with decreased 2-deoxy-D-glucose among all children. Among girls, third trimester concentrations of MECPP, MEHHP, MEHP, and MCPP were associated with 15, 13, 1, and 10 metabolites, respectively, including decreased choline and increased acylcarnitines and saturated FAs (FA). Among boys, third trimester MIBP was positively associated with 9 features including long chain saturated FAs, and second trimester MBzP was inversely associated with thyroxine.
Metabolomics biomarkers may reflect sex- and exposure timing-specific responses to prenatal phthalate exposures manifesting in childhood that may not be detected using standard clinical markers of cardiometabolic risk.
•Evidence suggests air pollution exposure may influence mental health.•We studied PM2.5 exposure in pregnancy and postpartum depression (PPD) risk.•In Mexico City, PM2.5 in pregnancy was associated ...with higher PPD risk at 6 months.•PM2.5 in pregnancy was also linked with 6-month anhedonia and depression scores.•Air pollution in pregnancy may influence maternal postpartum psychological function.
Postpartum depression (PPD), which affects up to 1 in 5 mothers globally, negatively impacts the health of both mothers and children. Exposure to ambient air pollution has been linked to depressive symptoms in animal models and human studies, but the relationship between air pollution and PPD has not been widely studied.
In a birth cohort in Mexico City (509 mothers with available data), we examined the association between exposure to particulate matter ≤2.5 μm in diameter (PM2.5) with symptoms of psychological dysfunction at 1 and 6 months postpartum. Daily PM2.5 estimates were derived from a hybrid satellite-based spatio-temporally resolved model and averaged over pregnancy and the first year postpartum. Edinburgh Postnatal Depression Scale (EPDS) scores at 1 and 6 months were used to assess the relationship between PM2.5 exposure and probable PPD (EPDS score ≥13) using relative risk regression and symptoms of anhedonia, depression, and anxiety (derived from EPDS subscales) using negative binomial regression.
A 5-μg/m3 increase in average PM2.5 exposure during pregnancy was associated with an increased risk of PPD at 6 months (RR = 1.59; 95% CI: 1.11 to 2.28) and of late-onset PPD (no PPD at 1 month, PPD at 6 months) (RR = 2.58; 95% CI: 1.40 to 4.73) in covariate-adjusted models. No association was observed between PM2.5 exposure in the first year postpartum and PPD. Average PM2.5 exposure during pregnancy was also associated with increased 6-month EPDS subscale symptom scores for anhedonia (p = 0.03) and depression (p = 0.04).
Our results suggest that in women in Mexico City, particulate matter exposure during pregnancy is positively associated with PPD and symptoms of anhedonia and depression at 6 months postpartum. Future studies should examine mechanisms linking air pollution and other environmental exposures during pregnancy with postpartum psychological functioning.
•Phthalate mixture at pregnancy was associated with long-term insulin resistance.•Phthalate mixture at pregnancy was associated with long term adverse lipid profiles.•Associations with glycemia ...biomarkers were primarily driven by MECPTP and ∑DBP.•Associations with lipid biomarkers were primarily driven by MECPTP, ∑DBP, and MEP.•Pregnancy phthalates exposure may be associated with long-term metabolic health.
Pregnancy induces numerous cardiovascular and metabolic changes. Alterations in these sensitive processes may precipitate long-term post-delivery health consequences. Studies have reported associations between phthalates and metabolic complications of pregnancy, but no study has investigated metabolic outcomes beyond pregnancy.
To examine associations of exposure to phthalates during pregnancy with post-delivery metabolic health.
We quantified 15 urinary phthalate biomarker concentrations during the second and third trimesters among 618 pregnant women from Mexico City. Maternal metabolic health biomarkers included fasting blood measures of glycemia glucose, insulin, Homeostatic Model Assessment of Insulin Resistance HOMA-IR, % hemoglobin A1c (HbA1c%) and lipids (total, high-density lipoprotein (HDL), low-density lipoprotein (LDL) cholesterol, triglycerides), at 4–5 and 6–8 years post-delivery. To estimate the influence of the phthalates mixture, we used Bayesian weighted quantile sum regression and Bayesian kernel machine regression; for individual biomarkers, we used linear mixed models.
As a mixture, higher urinary phthalate biomarker concentrations during pregnancy were associated with post-delivery concentrations of plasma glucose (interquartile range IQR difference: 0.13 SD, 95%CrI: 0.05, 0.20), plasma insulin (IQR difference: 0.06 SD, 95%CrI: −0.02, 0.14), HOMA-IR (IQR difference: 0.08 SD, 95% CrI: 0.01, 0.16), and HbA1c% (IQR difference: 0.15 SD, 95%CrI: 0.05, 0.24). Associations were primarily driven by mono-2-ethyl-5-carboxypentyl terephthalate (MECPTP) and the sum of dibutyl phthalate biomarkers (∑DBP). The phthalates mixture was associated with lower HDL (IQR difference: −0.08 SD, 95%CrI: −0.16, −0.01), driven by ∑DBP and monoethyl phthalate (MEP), and higher triglyceride levels (IQR difference: 0.15 SD, 95%CrI: 0.08, 0.22), driven by MECPTP and MEP. The overall mixture was not associated with total cholesterol and LDL. However, ∑DBP and MEP were associated with lower and higher total cholesterol, respectively, and MECPTP and ∑DBP were associated with lower LDL.
Phthalate exposure during pregnancy is associated with adverse long-term changes in maternal metabolic health. A better understanding of timing of the exact biological changes and their implications on metabolic disease risk is needed.
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•Translational research is limited in environmental toxicology and epidemiology.•Perinatal DEHP and Pb exposure induces epigenetic (DNA methylation) changes in mice.•Homologous human ...gene methylation is altered after prenatal DEHP and Pb exposure.•Translational toxicoepigenetics can identify consistent cross-species effects.
Although toxicology uses animal models to represent real-world human health scenarios, a critical translational gap between laboratory-based studies and epidemiology remains. In this study, we aimed to understand the toxicoepigenetic effects on DNA methylation after developmental exposure to two common toxicants, the phthalate di(2-ethylhexyl) phthalate (DEHP) and the metal lead (Pb), using a translational paradigm that selected candidate genes from a mouse study and assessed them in four human birth cohorts. Data from mouse offspring developmentally exposed to DEHP, Pb, or control were used to identify genes with sex-specific sites with differential DNA methylation at postnatal day 21. Associations of human infant DNA methylation in homologous mouse genes with prenatal DEHP or Pb were examined with a meta-analysis. Differential methylation was observed on 6 cytosines (adjusted-p < 0.05) and 90 regions (adjusted-p < 0.001). This translational approach offers a unique method that can detect conserved epigenetic differences that are developmentally susceptible to environmental toxicants.
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