Dataset Information

Prenatal traffic-related air pollution exposures, cord blood adipokines and infant weight.

ABSTRACT: OBJECTIVE:Studies suggest that prenatal exposure to traffic-related air pollution (TRAP) may contribute to childhood obesity. While exact mechanisms for this association are unknown, circulating adipokines are hypothesized to contribute to early-life weight gain. METHODS:The Maternal and Child Health Study birth cohort included 136 women from the Los Angeles County + University of Southern California Medical Center. This study estimated prenatal residential TRAP exposure and used linear regression analysis to examine associations between adipokines with TRAP exposure and infant weight change (birth to 6 months). RESULTS:A one standard deviation (1-SD: 2 ppb) increase in prenatal non-freeway nitrogen oxides was associated with 33% (P = 0.01) higher leptin and 9% higher high molecular weight adiponectin levels (P = 0.07) in cord blood. Leptin levels were 71% higher in mothers who lived <75 m than those living >300 m from major roadways (P = 0.03). A 1-SD (10 ng mL-1 ) increase in leptin was associated with a significant increase in infant weight change in female infants (0.62 kg, P = 0.02) but not male infants (0.11 kg, P = 0.48). CONCLUSIONS:Higher TRAP exposures were associated with higher cord blood levels of leptin and high molecular weight adiponectin. These adipokines were associated with increased infant weight change in female infants, which may have implications for future obesity risk.

SUBMITTER: Alderete TL

PROVIDER: S-EPMC5934325 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature

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Prenatal traffic-related air pollution exposures, cord blood adipokines and infant weight.

Alderete T L TL Song A Y AY Bastain T T Habre R R Toledo-Corral C M CM Salam M T MT Lurmann F F Gilliland F D FD Breton C V CV

Pediatric obesity 20171103 6

<h4>Objective</h4>Studies suggest that prenatal exposure to traffic-related air pollution (TRAP) may contribute to childhood obesity. While exact mechanisms for this association are unknown, circulating adipokines are hypothesized to contribute to early-life weight gain.<h4>Methods</h4>The Maternal and Child Health Study birth cohort included 136 women from the Los Angeles County + University of Southern California Medical Center. This study estimated prenatal residential TRAP exposure and used ...[more]

PMID: 29098799

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Project description:BACKGROUND:Prenatal exposures to ambient air pollution and traffic have been associated with adverse birth outcomes, and may also lead to an increased risk of obesity. Obesity risk may be reflected in changes in body composition in infancy. OBJECTIVE:To estimate associations between prenatal ambient air pollution and traffic exposure, and infant weight and adiposity in a Colorado-based prospective cohort study. METHODS:Participants were 1125 mother-infant pairs with term births. Birth weight was recorded from medical records and body composition measures (fat mass, fat-free mass, and adiposity [percent fat mass]) were evaluated via air displacement plethysmography at birth (n = 951) and at ~5 months (n = 574). Maternal residential address was used to calculate distance to nearest roadway, traffic density, and ambient concentrations of fine particulate matter (PM2.5) and ozone (O3) via inverse-distance weighted interpolation of stationary monitoring data, averaged by trimester and throughout pregnancy. Adjusted linear regression models estimated associations between exposures and infant weight and body composition. RESULTS:Participants were urban residents and diverse in race/ethnicity and socioeconomic status. Average ambient air pollutant concentrations were generally low; the median, interquartile range (IQR), and range of third trimester concentrations were 7.3 ?g/m3 (IQR: 1.3, range: 3.3-12.7) for PM2.5 and 46.3 ppb (IQR: 18.4, range: 21.7-63.2) for 8-h maximum O3. Overall there were few associations between traffic and air pollution exposures and infant outcomes. Third trimester O3 was associated with greater adiposity at follow-up (2.2% per IQR, 95% CI 0.1, 4.3), and with greater rates of change in fat mass (1.8 g/day, 95% CI 0.5, 3.2) and adiposity (2.1%/100 days, 95% CI 0.4, 3.7) from birth to follow-up. CONCLUSIONS:We found limited evidence of an association between prenatal traffic and ambient air pollution exposure and infant body composition. Suggestive associations between prenatal ozone exposure and early postnatal changes in body composition merit further investigation.

Project description:BACKGROUND:Residential proximity to major roadways, and prenatal exposures to particulate matter <2.5??m (PM2.5) 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 PM2.5 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 PM2.5 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 PM2.5 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 PM2.5 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??g/m3 increase in PM2.5 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 PM2.5 exposures. CONCLUSIONS:In this prospective cohort study, proximity to major roadway and prenatal/early-life exposures to PM2.5 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.

Project description:BackgroundTraffic-related air pollution exposure may influence brain development and function and thus be related to neurobehavioral problems in children, but little is known about windows of susceptibility.AimsExamine associations of gestational and childhood exposure to traffic-related pollution with executive function and behavior problems in children.MethodsWe studied associations of pre- and postnatal pollution exposures with neurobehavioral outcomes in 1212 children in the Project Viva pre-birth cohort followed to mid-childhood (median age 7.7years). Parents and classroom teachers completed the Behavior Rating Inventory of Executive Function (BRIEF) and the Strengths and Difficulties Questionnaire (SDQ). Using validated spatiotemporal models, we estimated exposure to black carbon (BC) and fine particulate matter (PM2.5) in the third trimester of pregnancy, from birth to 3years, from birth to 6years, and in the year before behavioral ratings. We also measured residential distance to major roadways and near-residence traffic density at birth and in mid-childhood. We estimated associations of BC, PM2.5, and other traffic exposure measures with BRIEF and SDQ scores, adjusted for potential confounders.ResultsHigher childhood BC exposure was associated with higher teacher-rated BRIEF Behavioral Regulation Index (BRI) scores, indicating greater problems: 1.0 points (95% confidence interval (CI): 0.0, 2.1) per interquartile range (IQR) increase in birth-age 6BC, and 1.7 points (95% CI: 0.6, 2.8) for BC in the year prior to behavioral ratings. Mid-childhood residential traffic density was also associated with BRI score (0.6, 95% CI: 0.1, 1.1). Birth-age 3BC was not associated with BRIEF or SDQ scores. Third trimester BC exposure was not associated with teacher-rated BRI scores (-0.2, 95% CI: -1.1, 0.8), and predicted lower scores (fewer problems) on the BRIEF Metacognition Index (-1.2, 95% CI: -2.2, -0.2) and SDQ total difficulties (-0.9, 95% CI: -1.4, -0.4). PM2.5 exposure was associated with teacher-rated BRIEF and SDQ scores in minimally adjusted models but associations attenuated with covariate adjustment. None of the parent-rated outcomes suggested adverse effects of greater pollution exposure at any time point.ConclusionsChildren with higher mid-childhood exposure to BC and greater near-residence traffic density in mid-childhood had greater problems with behavioral regulation as assessed by classroom teachers, but not as assessed by parents. Prenatal and early childhood exposure to traffic-related pollution did not predict greater executive function or behavior problems; third trimester BC was associated with lower scores (representing fewer problems) on measures of metacognition and behavioral problems.

Dataset Information

Prenatal traffic-related air pollution exposures, cord blood adipokines and infant weight.

Publications

Prenatal traffic-related air pollution exposures, cord blood adipokines and infant weight.

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