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

Previous research has revealed links between air pollution exposure and metabolic syndrome in adults; however, these associations are less explored in children.

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.

We conducted cross-sectional analyses in a sample of predominantly Latinx, low-income children (n = 218) to examine associations between air pollutants (nitrogen dioxide (NO₂), 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)).

HDL cholesterol showed an inverse association with NO₂ and NO_x, with the strongest relationship between HDL and 3-month exposure to NO₂ (-15.4 mg/dL per IQR increase in 3-month NO₂, 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.

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.