Introduction: Cardiovascular disease disproportionately affects individuals of lower socioeconomic position, partly due to higher exposure to environmental pollutants such as traffic-related air pollution (TRAP). TRAP has been associated with amplified autonomic responses, but the mechanisms linking pollutant exposure to stress-induced cardiovascular dysfunction remain unclear. We hypothesized that TRAP-induced inflammatory signaling exaggerates cardiovascular responses to acute stress. Methods: Thirteen-week-old Sprague Dawley rats of both sexes were exposed for three weeks to real-time TRAP collected from the Caldecott Tunnel in California. Bore 1 (HDV) included heavy- and light-duty vehicles, while Bore 2 (LDV) was restricted to light-duty vehicles. Serum samples (n = 84) were collected at the end of each week to quantify circulating cytokines using ELISA. Blood pressure and electrocardiograms were recorded via telemetry (n = 24). Stress groups underwent 1-hour immobilization restraint in weeks 2 and 3 to assess acute stress responses and adaptation to repeated stress. Results: TRAP exposure, at concentrations near Environmental Protection Agency ambient air quality standards, reduced circulating cytokine concentrations in both LDV and HDV groups, with LDV rats showing a modest increase at week 2 before declining by week 3. During the first restraint, filter-air (FA) controls exhibited increases in only a few cytokines (GRO/KC, RANTES, MCP-1), whereas LDV exposure suppressed most cytokines and HDV exposure induced broad increases. In the second restraint, FA rats showed overall cytokine reductions; LDV rats exhibited increases in IL-6, G-CSF, IL-13, IFN-ɣ, and TNF-α; and HDV rats displayed attenuated responses relative to the first restraint. TRAP exposure consistently amplified pressor and tachycardia responses to restraint, with HDV rats showing the strongest and FA controls the weakest cardiovascular responses. Peak responses were comparable between restraints, indicating no adaptation to repeated stress. Conclusion: TRAP exposure dampens resting inflammatory mediators while exaggerating stress-induced cytokine and cardiovascular responses. These findings suggest that TRAP modifies the physiological response to acute stress, revealing a potential pathway through which environmental exposures contribute to long-term cardiovascular risk. Support: R01ES033472-01A1 & P30 ES023513 This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Leon et al. (Fri,) studied this question.