Abstract

Background: Limited evidence suggests an association between prenatal exposure to traffic pollution and greater adiposity in childhood, but the time window during which growth may be most affected is not known.Methods: We studied 1,649 children in Project Viva, a Boston-area pre-birth cohort. We used spatiotemporal models to estimate prenatal residential air pollution exposures and geographic information systems to estimate neighborhood traffic density and roadway proximity. We used weight and stature measurements at clinical and research visits to estimate a BMI trajectory for each child with mixed-effects natural cubic spline models. In primary analyses, we examined associations of residential PM2.5 and black carbon (BC) exposures during the third trimester and neighborhood traffic density and home roadway proximity at birth address with (1) estimated BMI at 6 month intervals through 10 years of age, (2) magnitude and timing of BMI peak and rebound, and (3) overall BMI trajectory. In secondary analyses, we examined associations of residential PM2.5 and BC exposures during the first and second trimesters with BMI outcomes.Results: Median (interquartile range; IQR) concentration of residential air pollution during the third trimester was 11.4 (1.7) μg/m3 for PM2.5 and 0.7 (0.3) μg/m3 for BC. Participants had a median (IQR) of 13 (7) clinical or research BMI measures from 0 to 10 years of age. None of the traffic pollution exposures were significantly associated with any of the BMI outcomes in covariate-adjusted models, although effect estimates were in the hypothesized direction for neighborhood traffic density and home roadway proximity. For example, greater neighborhood traffic density [median (IQR) 857 (1,452) vehicles/day x km of road within 100 m of residential address at delivery] was associated with a higher BMI throughout childhood, with the strongest associations in early childhood [e.g., per IQR increment natural log-transformed neighborhood traffic density, BMI at 12 months of age was 0.05 (−0.03, 0.13) kg/m2 higher and infancy peak BMI was 0.05 (−0.03, 0.14) kg/m2 higher].Conclusions: We found no evidence for a persistent effect of prenatal exposure to traffic pollution on BMI trajectory from birth through mid-childhood in a population exposed to modest levels of air pollution.

Highlights

  • Childhood obesity often tracks into adulthood [1], leading to costly comorbidities and lower life expectancy in affected individuals [2]

  • Despite the fact that obesity is more prevalent as children age [20], there has been no prior evaluation of the extent to which prenatal traffic pollution exposure may differentially impact growth at different time windows during childhood

  • Because we have previously shown 3rd trimester exposure to traffic pollution to be most closely associated with fetal and infant growth in Project Viva [12], in primary analyses, we used estimates of residential traffic pollution during the 3rd trimester, which we obtained by averaging daily exposures from the 188th day (i.e.—27 weeks gestation) after the last menstrual period (LMP) to the day before birth

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Summary

Introduction

Childhood obesity often tracks into adulthood [1], leading to costly comorbidities and lower life expectancy in affected individuals [2]. Early life air pollution exposure results in systemic and adipose inflammation and leads to greater visceral adiposity [5]. Consistent with this observation, epidemiologic studies have demonstrated an association between air pollution exposure during childhood and increased risk of overweight or obesity [6,7,8,9,10]. Prenatal air pollution may affect child weight directly by increasing inflammatory potential of fetal adipose tissue or indirectly by restricting fetal growth or disrupting maternal glycemia, which have both been associated with prenatal air pollution exposure in our cohort [11, 12] and others [16, 17] and may prime children for greater weight or adiposity later in life [18, 19]. Limited evidence suggests an association between prenatal exposure to traffic pollution and greater adiposity in childhood, but the time window during which growth may be most affected is not known

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