Thus, use of these surrogate vascular markers, which represent some of the best early biomarkers of adverse outcomes available in youth, may help to develop a better understanding of early vascular changes and their correlates and may also facilitate identification of children at risk for cardiovascular disease later in life. Plenty of evidence exists linking endothelial dysfunction to the later development of clinical vascular disease. CAS, in fact, may be viewed as an early biomarker of endothelial function in which observed abnormalities reflect changes in the integrity of the vascular structure prior to manifestation of symptomatic cardiovascular events. Whether changes in CAS in children predict adult cardiovascular risk remains unknown, although recent evidence suggests blood pressure and CAS are highly related and childhood blood pressure tracks closely with adult blood pressure, increasing later cardiovascular risk. Changes in CAS, in particular, may reflect both the structural and functional health of the arterial vasculature. Long-term exposures have been associated with measures of atherosclerosis, including carotid intima-media thickness (CIMT) and arterial stiffness (CAS), both of which predict future cardiovascular events in adults. The negative health effects of air pollution exposure on cardiovascular risk are well documented in adults. Efforts aimed at limiting prenatal exposures are important public health goals. In conclusion, prenatal exposure to elevated air pollutants may increase carotid arterial stiffness in a young adult population of college students. Mutually adjusted models of pre- and postnatal PM 2.5 further suggested the prenatal exposure was most relevant exposure period for CAS. For example, a 2 SD increase in prenatal PM 2.5 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. Prenatal PM 10 and PM 2.5 exposures were associated with increased CAS. The associations between CAS, CIMT and air pollutants were assessed using linear regression analysis. Environmental Protection Agency’s Air Quality System (AQS) database. Prenatal residential addresses were geocoded and used to assign prenatal and postnatal air pollutant exposure estimates using the U.S. 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. The Testing Responses on Youth (TROY) study consists of 768 college students recruited from the University of Southern California in 2007–2009. We aimed to evaluate the contribution of prenatal air pollutant exposure to cardiovascular health, which has not been thoroughly evaluated. Exposure to ambient air pollutants increases risk for adverse cardiovascular health outcomes in adults.
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