The proposed study addresses the need for the improved understanding of the impact of transient and longer- term exposure to particulate matter present in urban air pollution on the cardiovascular health of children. Specifically, it wil investigate the hypothesis that transient exposure to high PM2.5 and UFP levels promotes oxidative stress and systemic inflammation in children. The study also will examine the hypothesis that chronic PM exposure promotes vascular remodeling (via systemic inflammation) in the form of increased arterial stiffness and thickness. It is hypothesized that the adverse cardiovascular effects of PM exposure will be accelerated in the presence of other pro-inflammatory factors (e.g., obesity, high fat diet, sedentarism) while anti-inflammatory factors wil act to reduce these (e.g., diet rich in fresh fruits and vegetables). The study will be conducted i 300 children (age 7-11 yrs) residing in the El Paso, Texas. The geographic characteristics, and presence of US Interstate 10, the second largest port of entry on the US-Mexico border and 200 factories cause some neighborhoods to be heavily polluted than others. To investigate the effects of transient exposure to ambient PM2.5 and UFP with systemic inflammation indicators in healthy children, a 2-wave panel study will be carried out in three (high, medium and low PM) neighborhoods to investigate the association of transient PM2.5 and UFP exposure with inflammation as measured by hpCRP, IL-6, isoprostane, ICAM-1, VCAM-1, and P-selectin adhesion molecules. Before each of the two inflammatory biomarker blood draws, five cumulative exposure measurements will be constructed for each prior 60-day period (prior day, 2-days, week, month, and 2-month average). Spatial-temporal models of cumulative long-term (5 yr) PM2.5 and UFP exposures will be constructed for five different exposure measures (prior 12, 24, 36, 48, and 60 mos. average). Exposure models for both panel and long-term PM studies will be constructed from central air quality monitors located in the three target neighborhoods. Portable PM monitors placed outside schools and in strategic neighborhood locations will be used to identify PM sources and composition. Other portable monitors placed inside the three neighborhood schools and from a random subsample of participants and their homes will collect data on indoor and personal PM exposure. These data will be used to adjust for measurement error in the PM exposure models. The multivariate statistical models will also consider the contributions of pollutant gases, weather conditions, and other potential covariates. To investigate whether chronic exposure to high PM2.5 and UFP is associated with indicators of vascular remodeling, during the first study wave, participants will also undergo ultrasound studies. These to examine the relationship of chronic PM2.5 and UFP exposure with blood endothelin-1 levels, arterial thickening measured by abdominal (aIMT) and carotid (cIMT) intima-media thickness and arterial stiffness (brachial artery flow-mediated dilation). To identify the elemental composition (e.g., hydrocarbons, quinines, light cations, heavy and transition metals) and sources of outdoor PM2.5 and UFP present within each of the three neighborhood zones, ambient PM samples will be collected over a 12- month period at the three participating schools, their surrounding neighborhoods, and in a random sample of participant homes. The samples will be analyzed using an automated energy dispersive XRF instrument. .
The proposed study will investigate the hypothesis that children (7-11 years) who are chronically exposed to urban air pollutants experience oxidative stress and systemic inflammation that leads detectable arterial wall thickening and stiffening. The study also will examine elements present in PM that promote inflammation. The findings will help to better understand how urban air pollutants promote atherogenesis in children.