Abstract
Background: Increasing evidence suggests that exposure to air pollution during pregnancy is associated with adverse pregnancy outcomes. However, biomarkers associated with air pollution exposure are widely lacking and often transient. In addition, ascertaining biospecimens during pregnacy to assess the prenatal environment remains largely infeasible.Objectives: To address these challenges, we investigated relationships between air pollution exposure during pregnancy and human serum albumin Cys34 (HSA-Cys34) adducts in newborn dried blood spots (DBS) samples, which captures an integration of perinatal exposures to small reactive molecules in circulating blood.Methods: Newborn DBS were obtained from a state archive for a cohort of 120 children born at one Kaiser Permanente Southern California (KPSC) hospitals in 2007. These children were selected to maximize the range of residential air pollution exposure during the entire pregnancy to PM2.5, PM10, NO2, O3, based on monthly estimates interpolated from regulatory monitoring sites. HSA-Cys34 adducts were selected based on previously reported relationships with air pollution exposure and oxidative stress.Results: Six adducts measured in newborn DBS samples were associated with air pollution exposures during pregnancy; these included direct oxidation products, adducts formed with small thiol compounds, and adducts formed with reactive aldehydes. Two general trends were identified: Exposure to air pollution late in pregnancy (i.e., in the last 30 days) was associated with increased oxidative stress, and exposure to air pollution earlier in pregnancy (i.e., not in the last 30 days) was associated with decreased oxidative stress around the time of birth.Discussion: Air pollution exposure occurring during pregnancy can alter biology and leave measurable impacts on the developing infant captured in the newborn DBS adductome, which represents a promising tool for investigating adverse birth outcomes in population-based studies.
Highlights
Periods of fetal development and early childhood have long been recognized as a critical window of vulnerability for exposure to a number of environmental chemicals [1, 2], and higher prenatal exposures have been associated with adverse postnatal effects for many common pollutants [1,2,3]
While the underlying biological mechanisms linking air pollution and adverse birth outcomes are complex and are not fully understood, oxidative stress and inflammation are thought to play a central role in air pollution toxicity through the generation of reactive oxygen species (ROS) [18,19,20], altered antioxidant defense, and disruptions in homeostatic processes [19,20,21]
Air pollution exposure during the last 30 days of pregnancy was associated with decreased S-sulfinic acid, decreased S-γ -GluCys, and increased S-crotonaldehyde, which are all consistent with increased levels oxidative stress
Summary
Periods of fetal development and early childhood have long been recognized as a critical window of vulnerability for exposure to a number of environmental chemicals [1, 2], and higher prenatal exposures have been associated with adverse postnatal effects for many common pollutants [1,2,3]. Increasing evidence suggests that exposure to certain air pollutants during pregnancy may be associated with adverse pregnancy outcomes including preterm birth [4,5,6,7], low birth weight [4,5,6,7,8], intrauterine growth restriction [4, 9, 10], congenital anomalies [11, 12], and autism spectrum disorders [13,14,15,16]. Associations between air pollution exposures and adverse birth outcomes remain poorly understood due to the paucity of in vivo markers of effects. Increasing evidence suggests that exposure to air pollution during pregnancy is associated with adverse pregnancy outcomes. Ascertaining biospecimens during pregnacy to assess the prenatal environment remains largely infeasible
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