Relationship between traffic-related air pollution and inflammation biomarkers using structural equation modeling.

Background: Evidence suggests that exposure to traffic-related air pollution (TRAP) and social stressors can increase inflammation. Given that there are many different markers of TRAP exposure, socio-economic status (SES), and inflammation, analytical approaches can leverage multiple markers to better elucidate associations. In this study, we applied structural equation modeling (SEM) to assess the association between a TRAP construct and a SES construct with an inflammation construct.

Methods: This analysis was conducted as part of the Community Assessment of Freeway Exposure and Health (CAFEH; N = 408) study. Air pollution was characterized using a spatiotemporal model of particle number concentration (PNC) combined with individual participant time-activity adjustment (TAA). TAA-PNC and proximity to highways were considered for a construct of TRAP exposure. Participant demographics on education and income for an SES construct were assessed via questionnaires. Blood samples were analyzed for high sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), and tumor necrosis factor-α receptor II (TNFRII), which were considered for the construct for inflammation. We conducted SEM and compared our findings with those obtained using generalized linear models (GLM).

Results: Using GLM, TAA-PNC was associated with multiple inflammation biomarkers. An IQR (10,000 particles/cm) increase of TAA-PNC was associated with a 14 % increase in hsCRP in the GLM. Using SEM, the association between the TRAP construct and the inflammation construct was twice as large as the associations with any individual inflammation biomarker. SES had an inverse association with inflammation in all models. Using SEM to estimate the indirect effects of SES on inflammation through the TRAP construct strengthened confidence in the association of TRAP with inflammation.

Conclusion: Our TRAP construct resulted in stronger associations with a combined construct for inflammation than with individual biomarkers, reinforcing the value of statistical approaches that combine multiple, related exposures or outcomes. Our findings are consistent with inflammatory risk from TRAP exposure.