Adverse childhood experiences (ACEs) moderate the association between traffic exposure and circulating inflammatory biomarkers.

Although traffic-related air pollution and early-life adversity have both been related to increased inflammatory activity and cardiovascular disease, rarely have these two risk factors been examined together. To address this issue, we investigated whether adverse childhood experiences (ACEs) moderate associations between residential traffic exposure and inflammatory biomarkers linked to cardiovascular risk. We analyzed data from 274 nursing students in the Nurse Engagement and Wellness Study, and assessed interactions between ACE scores and residential traffic exposure (quantified using Vehicle Miles Traveled across different buffers) on the inflammatory markers C-reactive protein and serum amyloid P. Using Johnson-Neyman intervals, we identified specific regions of the ACE score continuum where significant moderation occurred. Results showed that ACE exposure significantly moderated the association between traffic exposure and inflammation. Moreover, individuals with higher early-life stress (≥4 ACEs) exhibited amplified inflammatory responses to traffic exposure. At the 250 m buffer, a 10% increase in traffic exposure was associated with a 1.0% relative increase in CRP among participants with 4 ACEs, increasing to a 3.4% relative increase among those with 10 ACEs. We found similar dose-dependent patterns for SAP. Together, these findings suggest that early adversity increases susceptibility to traffic-related inflammatory activity. Addressing psychosocial and environmental exposures simultaneously may thus be critical for reducing cardiovascular risk.