Prenatal Air Pollution Exposure and Early Cardiovascular Phenotypes in Young Adults.

Carrie V Breton,Howard N Hodis,Frank Gilliland,Rob Mcconnell,Fred Lurmann,Kiros Berhane,Wendy J Mack,Jin Yao,Milena Amadeus,Nino Künzli,Ed Avol,Rudolf Kirchmair

doi:10.1371/journal.pone.0150825

Abstract

Exposure to ambient air pollutants increases risk for adverse cardiovascular health outcomes in adults. We aimed to evaluate the contribution of prenatal air pollutant exposure to cardiovascular health, which has not been thoroughly evaluated. The Testing Responses on Youth (TROY) study consists of 768 college students recruited from the University of Southern California in 2007–2009. Participants attended one study visit during which blood pressure, heart rate and carotid artery arterial stiffness (CAS) and carotid artery intima-media thickness (CIMT) were assessed. Prenatal residential addresses were geocoded and used to assign prenatal and postnatal air pollutant exposure estimates using the U.S. Environmental Protection Agency’s Air Quality System (AQS) database. The associations between CAS, CIMT and air pollutants were assessed using linear regression analysis. Prenatal PM10 and PM2.5 exposures were associated with increased CAS. For example, a 2 SD increase in prenatal PM2.5 was associated with CAS indices, including a 5% increase (β = 1.05, 95% CI 1.00–1.10) in carotid stiffness index beta, a 5% increase (β = 1.05, 95% CI 1.01–1.10) in Young’s elastic modulus and a 5% decrease (β = 0.95, 95% CI 0.91–0.99) in distensibility. Mutually adjusted models of pre- and postnatal PM2.5 further suggested the prenatal exposure was most relevant exposure period for CAS. No associations were observed for CIMT. In conclusion, prenatal exposure to elevated air pollutants may increase carotid arterial stiffness in a young adult population of college students. Efforts aimed at limiting prenatal exposures are important public health goals.

Highlights

The negative health effects of air pollution exposure on cardiovascular risk are well documented in adults [1,2,3]
Animal models of prenatal exposure to pollutants and to tobacco smoke have demonstrated increased cardiac oxidative stress and atherogenesis in adult mice [20,21]. Pollutants such as PM2.5 have been associated with systemic inflammation, oxidative stress, and endothelial injury in children and young adults [22,23,24]. To address this lack of knowledge, we investigated the association between prenatal trimester-specific and postnatal exposures to PM10, PM2.5, NO2 and O3 with carotid artery arterial stiffness (CAS) and carotid intima-media thickness (CIMT) in a population of University of Southern California (USC) college students
Because we previously reported an association between early childhood, elementary school and lifetime air pollution exposures with CIMT in this cohort [6], we investigated these postnatal exposure windows with CAS

Summary

Introduction

The negative health effects of air pollution exposure on cardiovascular risk are well documented in adults [1,2,3]. Long-term exposures have been associated with measures of atherosclerosis, including carotid intima-media thickness (CIMT) and arterial stiffness (CAS), PLOS ONE | DOI:10.1371/journal.pone.0150825. STI was paid to conduct the air pollution exposure assignments used in the analyses in this manuscript. The specific roles of these authors are articulated in the ‘author contributions’ section.

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