Abstract

Background: Potential synergy between childhood exposure to psychosocial stressors and traffic-related air pollution exposure, two factors that commonly overlap in socially disadvantaged groups, could increase the risk of cardiovascular disease and lead to greater health disparity than what is currently attributed to these factors independently. Aim: To test whether adverse childhood experiences (ACEs) potentiate the response of retinal microvasculature caliber and circulatory pro-inflammatory cytokines following a two-hour semi-controlled exposure to traffic related air pollution. Method: In a crossover experiment, 57 participants were exposed to near-traffic ambient air and filtered ambient air, in separate occasions for two hours each time. Central retinal arteriolar/venular equivalent (CRAE/CRVE), blood pressure, pulse, and circulating interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α (TNF-α) were measured pre-exposure and, again, 1 hour and 24 hours post-exposure. ACEs were documented using the ACE questionnaire. Based on ACE scores, participants were grouped into high (ACE ≥ 4) and low (ACE ≤ 1) ACE groups. Microvascular and inflammatory response to the exposure were analyzed across groups. Results: ACE scores significantly predicted CRAE, IL-6, IL-8, and pulse reactivity. Left eye CRAE narrowing was greater in the high- vs. low-ACE group at 1-hour and 24-hours post-exposure. 24-hours post-exposure, IL-8 and pulse were significantly higher in the high- vs. low-ACE group. IL-6 was significantly lower in the high- vs. low-ACE group at 1-hour post-exposure. Conclusion: Our results support the hypothesis that ACEs may induce susceptibility to air pollution across the lifespan. These findings may thus help explain how health disparities develop and persist across the lifespan in persons who are most vulnerable to experiencing ACEs and poor air quality, leading to continued social disadvantage.

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