RESUMO
OBJECTIVE: To examine relationships between traffic-related air pollution (TRAP) and markers of pre-clinical cardiovascular risk in young children. STUDY DESIGN: We studied a cohort of healthy children ages 2-5 recruited from pediatric primary care sites (n = 122). We obtained child weight, height, blood pressure and hair nicotine levels. A blood sample was obtained for biomarkers of systemic inflammation, oxidation, and prevalence of circulating endothelial progenitor cells. This manuscript represents a secondary analysis. TRAP exposure (particulate levels, nitrogen dioxide, nitrogen oxides, and proximity to major roadways) was assessed using national air pollution data based on child's census tract of residence. RESULTS: TRAP exposure had significant positive associations with prevalence of two of the three EPC subtypes (CD34 + /CD133 + /CD45- and CD133 + /CD45-) in unadjusted correlations. In a linear regression model, adjusting for sex, age, race, ethnicity, body mass index, parental education, child insurance, and secondhand smoke exposure, one EPC subtype (CD133 + /CD45-) had a positive significant correlation to every TRAP measure. No significant relationships between air pollution and measures of inflammation and oxidation was found. CONCLUSION: Our findings of the upregulation of EPCs may signal a response to early vascular damage during early childhood due to air pollution exposure. IMPACT: Traffic-related air pollution (TRAP) - known cardiovascular risk factor during adulthood Current pilot study in very young children shows upregulation of cells which protect the endothelial lining of blood vessels (endothelial progenitor cells, EPCs) Upregulation of EPCs aligns with other cardiovascular risks during childhood (obesity, prematurity, type 1 diabetes) Demonstrated with TRAP exposure lower than EPA threshold Response to air pollution may be protective of cardiovascular damage during early childhood.