Prenatal Exposure to Ambient Air Pollutants and Infant Growth Among Hispanics from Southern California

Abstract

Background: Prior epidemiological and animal work has linked in utero exposure to ambient air pollutants (AAP) with accelerated postnatal weight gain. The objective of this study was to examine relationships between prenatal residential AAP exposure with infant growth.Methods: Residential exposure to AAP (particulate matter <2.5 and 10 microns in aerodynamic diameter [PM2.5, PM10]; nitrogen dioxide [NO2]; ozone [O3]; oxidative capacity [Ox: redox-weighted oxidative potential of O3 and NO2]) was modeled for 123 participants from the longitudinal Mother’s Milk Study, an ongoing cohort of Hispanic mother-infant dyads from Southern California. Multivariate linear regression was performed to examine the relationships between prenatal AAP exposure and changes in infant growth, skinfold measures, and predicted body fat and lean mass (calculated using infant demographics, anthropometrics, and EchoMRI from a subset) from 1-to-6 months of life. 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.Results: Higher NO2 was associated with a greater increase in infant weight (β=0.14, p=0.03), predicted lean mass (β=0.05, p=0.01), and midthigh skinfold thickness (β=0.84, p=0.03). PM10 and PM2.5 were positively associated with change in umbilical circumference (β=0.84, p=0.001 and β=0.56, p=0.04, respectively) and suprailiac skinfold thickness (β=0.38, p=0.02 and β=0.34, p=0.04, respectively). Lastly, Ox (pinteractions<0.02) was positively associated with change in umbilical circumference among females (β=1.23, p=0.001), but not males (β=-0.08, p=0.84) and was inversely associated with infant length change (β=-0.57, p=0.02) among males, but not females (β=0.17, p=0.48).Conclusion: Prenatal AAP exposure was associated with increased weight gain and anthropometric measures from 1-to-6 months of life. 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.