Abstract

BackgroundPrior epidemiological and animal work has linked in utero exposure to ambient air pollutants (AAP) with accelerated postnatal weight gain, which is predictive of increased cardiometabolic risk factors in childhood and adolescence. However, few studies have assessed changes in infant body composition or multiple pollutant exposures. Therefore, the objective of this study was to examine relationships between prenatal residential AAP exposure with infant growth and adiposity.MethodsResidential exposure to AAP (particulate matter < 2.5 and 10 microns in aerodynamic diameter [PM2.5, PM10]; nitrogen dioxide [NO2]; ozone [O3]; oxidative capacity [Oxwt: redox-weighted oxidative potential of O3 and NO2]) was modeled by spatial interpolation of monitoring stations via an inverse distance-squared weighting (IDW2) algorithm for 123 participants from the longitudinal Mother’s Milk Study, an ongoing cohort of Hispanic mother-infant dyads from Southern California. Outcomes included changes in infant growth (weight, length), total subcutaneous fat (TSF; calculated via infant skinfold thickness measures) and fat distribution (umbilical circumference, central to total subcutaneous fat [CTSF]) and were calculated by subtracting 1-month measures from 6-month measures. Multivariable linear regression was performed to examine relationships between prenatal AAP exposure and infant outcomes. Models adjusted for maternal age, pre-pregnancy body mass index, socioeconomic status, infant age, sex, and breastfeeding frequency. Sex interactions were tested, and effects are reported for each standard deviation increase in exposure.ResultsNO2 was associated with greater infant weight gain (β = 0.14, p = 0.02) and TSF (β = 1.69, p = 0.02). PM10 and PM2.5 were associated with change in umbilical circumference (β = 0.73, p = 0.003) and TSF (β = 1.53, p = 0.04), respectively. Associations of Oxwt (pinteractions < 0.10) with infant length change, umbilical circumference, and CTSF were modified by infant sex. Oxwt was associated with attenuated infant length change among males (β = -0.60, p = 0.01), but not females (β = 0.16, p = 0.49); umbilical circumference among females (β = 0.92, p = 0.009), but not males (β = -0.00, p = 0.99); and CTSF among males (β = 0.01, p = 0.03), but not females (β = 0.00, p = 0.51).ConclusionPrenatal AAP exposure was associated with increased weight gain and anthropometric measures from 1-to-6 months of life among Hispanic infants. Sex-specific associations suggest differential consequences of in utero oxidative stress. These results indicate that prenatal AAP exposure may alter infant growth, which has potential to increase childhood obesity risk.

Highlights

  • Prior epidemiological and animal work has linked in utero exposure to ambient air pollutants (AAP) with accelerated postnatal weight gain, which is predictive of increased cardiometabolic risk factors in childhood and adolescence

  • Patterson et al Environ Health (2021) 20:67 oxidative stress. These results indicate that prenatal AAP exposure may alter infant growth, which has potential to increase childhood obesity risk

  • Accelerated weight trajectory during the first six months of life has been linked to obesity at three years of age [4] and greater than expected weight gain during any period through four years of age has been found to be associated with increased body mass index (BMI) in adolescence [5]

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Summary

Introduction

Prior epidemiological and animal work has linked in utero exposure to ambient air pollutants (AAP) with accelerated postnatal weight gain, which is predictive of increased cardiometabolic risk factors in childhood and adolescence. Exposure to air pollutants during these periods is suggested as a risk factor for low birth weight, accelerated growth in early life, and/or childhood obesity [7,8,9,10,11]. This may partially explain the aforementioned disparities in childhood obesity, as Hispanics are exposed to higher levels of ambient (AAP) and traffic-related air pollutants [12, 13]

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