Dataset Information

Association of exposure to di-2-ethylhexylphthalate replacements with increased blood pressure in children and adolescents.

ABSTRACT: Phthalates are environmental chemicals widely used in consumer and personal care products. In this study, we examined associations of urinary phthalates with blood pressure, triglycerides, and lipoproteins in children and adolescents, performing a cross-sectional analysis of a subsample of US children 6 to 19 years of age who participated in the National Health and Nutrition Examination Survey between the years 2009 and 2012. We quantified exposure to common environmental phthalates, with a focus on the dietary contaminant di-2-ethylhexylphthalate and 2 increasingly used replacements, di-isononyl phthalate and di-isodecyl phthalate, based on micromolar concentration of urinary metabolites. We assessed descriptive, univariate, and multivariable associations with blood pressure and lipids. Controlling for an array of sociodemographic and behavioral factors, as well as diet and body mass, metabolites of di-2-ethylhexylphthalate, di-isononyl phthalate, and di-isodecyl phthalate were associated with higher age-, sex- and height-standardized blood pressure. For each log unit increase in di-isodecyl phthalate metabolites, a 0.105 standard deviation unit increase in systolic blood pressure z score was identified (P=0.004); for di-isononyl phthalate metabolites, a 0.113 standard deviation unit increment was identified (P=0.008). For di-2-ethylhexylphthalate metabolites, a 0.103 standard deviation unit increment (P=0.013) was detected. Metabolites of low molecular weight phthalates commonly found in cosmetics and personal care products showed an association with blood pressure (?90th percentile) in univariate analysis, but this was no longer significant in our full multivariable model, suggesting specificity. Phthalate metabolites were not associated with triglycerides or high-density lipoproteins. Further, longitudinal studies are needed to confirm these associations and to assess opportunities for intervention.

SUBMITTER: Trasande L

PROVIDER: S-EPMC4499862 | biostudies-literature | 2015 Aug

REPOSITORIES: biostudies-literature

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Association of exposure to di-2-ethylhexylphthalate replacements with increased blood pressure in children and adolescents.

Trasande Leonardo L Attina Teresa M TM

Hypertension (Dallas, Tex. : 1979) 20150801 2

Phthalates are environmental chemicals widely used in consumer and personal care products. In this study, we examined associations of urinary phthalates with blood pressure, triglycerides, and lipoproteins in children and adolescents, performing a cross-sectional analysis of a subsample of US children 6 to 19 years of age who participated in the National Health and Nutrition Examination Survey between the years 2009 and 2012. We quantified exposure to common environmental phthalates, with a focu ...[more]

PMID: 26156503

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Project description:BackgroundHigh blood pressure (BP) in childhood is frequently renal in origin and a risk factor for adult hypertension and cardiovascular disease. Shorter gestations are a known risk factor for increased BP in adults and children, due in part to a nephron deficit in children born preterm. As nephrogenesis is incomplete until 36 weeks gestation, prenatal lead exposure occurring during a susceptible period of renal development may contribute to programming for later life renal disease. The relationship between shorter gestation and children's BP has not yet been explored to identify i) critical windows using nonlinear piecewise models or ii) combined with other early life risk factors such as prenatal lead exposure.Objectives(1) To evaluate the nonlinear relationship between lower gestational age and childhood BP measured at 4-6 years of age, and (2) to investigate modification by prenatal lead exposure.MethodsIn a prospective longitudinal birth cohort, we assessed 565 children between 4 and 6 years of age (mean: 4.8 years) in the PROGRESS cohort in Mexico City, Mexico. Gestational age at delivery was calculated using maternal report of last menstrual period (LMP) and confirmed with Capurro physical examination at birth. We measured pregnant women's blood lead levels (BLLs) in the second trimester via inductively coupled plasma-mass spectrometry and children's BP using an automated device. We performed both linear and nonlinear piecewise regression analyses to examine associations of gestational age with children's BP adjusting for children's age, sex, height, prenatal exposure to smoke, and maternal socioeconomic status. We stratified to assess modification by prenatal lead exposure, and used a data-adaptive approach to identify a lead cutpoint.ResultsMaternal second trimester BLLs ranged from 0.7 to 17.8 μg/dL with 112 (20%) women above the CDC guideline level of 5 μg/dL. In adjusted linear regression models, a one week reduction in gestational age was associated with a 0.5 mm Hg (95%CI: 0.2, 0.8) increase in SBP and a 0.4 mm Hg (95%CI 0.1, 0.6) increase in DBP. Our nonlinear models suggested evidence for different magnitude estimates on either side of an estimated join-point at 35.9 weeks' gestation, but did not reach statistical significance. However, when stratified by prenatal lead exposure, we identified a cutpoint lead level of concern of 2.5 μg/dL that suggested an interaction between gestational age and blood lead. Specifically, for BLLs ≥ 2.5 μg/dL, SBP was 1.6 (95%CI: 0.3, 2.9) mm Hg higher per each week reduction in gestational age among children born before 37.0 weeks; and among children born after 37.0 weeks, this relationship was attenuated yet remained significant [β: 0.9, 95%CI (0.2, 1.6)]. At BLLs below 2.5 μg/dL, there was no appreciable association between lower gestational age and SBP.ConclusionsOur findings suggest that shorter gestation combined with higher prenatal lead exposure contributes to a higher risk of increased SBP at 4-6 years of age, particularly among infants born <37 weeks gestation. Our results underscore the importance of preventing prenatal lead exposure - even levels as low as 2.5 μg/dL - especially among pregnant women at risk for preterm birth. Given that high BP in childhood is a risk factor for adult hypertension and cardiovascular disease later in life, these results may have implications that extend across the life span.

Project description:Growing evidence suggests that environmental exposures can influence blood pressure over the course of a lifetime. Exposure to toxic metals, such as lead (Pb) and arsenic (As), has been associated with increased blood pressure in adults, but few studies have examined the impacts of in utero and early life toxic metals exposure on blood pressure in childhood. As subclinical vascular changes are thought to begin early in life, it is possible that in utero toxic metals exposure may play a role in blood pressure homeostasis. In the ongoing New Hampshire Birth Cohort Study, we investigated whether in utero exposure to Pb and As was associated with measures of blood pressure in a total of 323 young children (mean age 5.5 years, SD 0.4). Pb and As were measured in maternal toenail samples collected at ~28 weeks gestation (n = 257) and/or 6 weeks postpartum (n = 285), which represent exposures ~6 to 12 months prior to collection and therefore reflect the early prenatal and late prenatal exposures, respectively. Five measurements of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were averaged for each child using a standardized technique. In linear regression analyses, where log2-transformed prenatal toenail Pb and As were modeled jointly and adjusted for child age, sex, height, weight and maternal smoking during pregnancy, we observed that a doubling of maternal prenatal toenail Pb was associated with statistically significant increases in child SBP (β: 0.58 mm Hg, 95% CI: 0.05, 1.11). We did not observe any association of prenatal or postpartum As, or postpartum Pb, with SBP or DBP. Exploratory sex-stratified analyses suggest that associations of prenatal Pb with BP may be stronger among boys (SBP β: 0.72 mm Hg: 95% CI: -0.01, 1.44; DBP β: 0.37; 95% CI: -0.09, 0.84), compared to girls (SBP β: 0.48 mm Hg: 95% CI: -0.31, 1.26; DBP β: -0.05; 95% CI: -0.52, 0.41), though tests for interaction did not reach statistical significance (p-interaction SBP = 0.059; DBP = 0.057). Our preliminary results suggest that in utero toxic metals exposures may be associated with early life increases in blood pressure in children, which could have consequences for long-term health.

Project description:BackgroundChildhood exposure to air pollution contributes to cardiovascular disease in adulthood. Immune and oxidative stress disturbances might mediate the effects of air pollution on the cardiovascular system, but the underlying mechanisms are poorly understood in adolescents. Therefore, we aimed to identify immune biomarkers linking air pollution exposure and blood pressure levels in adolescents.MethodsWe randomly recruited 100 adolescents (mean age, 16 years) from Fresno, California. Using central-site data, spatial-temporal modeling, and distance weighting exposures to the participant's home, we estimated average pollutant levels [particulate matter (PM), polyaromatic hydrocarbons (PAH), ozone (O3), carbon monoxide (CO) and nitrogen oxides (NOx)]. We collected blood samples and vital signs on health visits. Using proteomic platforms, we quantitated markers of inflammation, oxidative stress, coagulation, and endothelial function. Immune cellular characterization was performed via mass cytometry (CyTOF). We investigated associations between pollutant levels, cytokines, immune cell types, and blood pressure (BP) using partial least squares (PLS) and linear regression, while adjusting for important confounders.ResultsUsing PLS, biomarkers explaining most of the variance in air pollution exposure included markers of oxidative stress (GDF-15 and myeloperoxidase), acute inflammation (C-reactive protein), hemostasis (ADAMTS, D-dimer) and immune cell types such as monocytes. Most of these biomarkers were independently associated with the air pollution levels in fully adjusted regression models. In CyTOF analyses, monocytes were enriched in participants with the highest versus the lowest PM2.5 exposure. In both PLS and linear regression, diastolic BP was independently associated with PM2.5, NO, NO2, CO and PAH456 pollution levels (P ≤ 0.009). Moreover, monocyte levels were independently related to both air pollution and diastolic BP levels (P ≤ 0.010). In in vitro cell assays, plasma of participants with high PM2.5 exposure induced endothelial dysfunction as evaluated by eNOS and ICAM-1 expression and tube formation.ConclusionsFor the first time in adolescents, we found that ambient air pollution levels were associated with oxidative stress, acute inflammation, altered hemostasis, endothelial dysfunction, monocyte enrichment and diastolic blood pressure. Our findings provide new insights on pollution-related immunological and cardiovascular disturbances and advocate preventative measures of air pollution exposure.

Dataset Information

Association of exposure to di-2-ethylhexylphthalate replacements with increased blood pressure in children and adolescents.

Publications

Association of exposure to di-2-ethylhexylphthalate replacements with increased blood pressure in children and adolescents.

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