Traffic-related air pollution, biomarkers of metabolic dysfunction, oxidative stress, and CC16 in children

Background Previous research has revealed links between air pollution exposure and metabolic syndrome in adults; however, these associations are less explored in children. Objective This study aims to investigate the association between traffic-related air pollutants (TRAP) and biomarkers of metabolic dysregulation, oxidative stress, and lung epithelial damage in children. Methods We conducted cross-sectional analyses in a sample of predominantly Latinx, low-income children ( n = 218) to examine associations between air pollutants (nitrogen dioxide (NO 2 ), nitrogen oxides (NO x ), elemental carbon, polycyclic aromatic hydrocarbons, carbon monoxide (CO), fine particulates (PM 2.5 )) and biomarkers of metabolic function (high-density lipoprotein (HDL), hemoglobin A1c (HbA1c), oxidative stress (8-isoprostane), and lung epithelial damage (club cell protein 16 (CC16)). Results HDL cholesterol showed an inverse association with NO 2 and NO x , with the strongest relationship between HDL and 3-month exposure to NO 2 (–15.4 mg/dL per IQR increase in 3-month NO 2 , 95% CI = –27.4, –3.4). 8-isoprostane showed a consistent pattern of increasing values with 1-day and 1-week exposure across all pollutants. Non-significant increases in % HbA1c were found during 1-month time frames and decreasing CC16 in 3-month exposure time frames. Conclusion Our results suggest that TRAP is significantly associated with decreased HDL cholesterol in longer-term time frames and elevated 8-isoprostane in shorter-term time frames. TRAP could have the potential to influence lifelong metabolic patterns, through metabolic effects in childhood.