Abstract 20747: Systolic Blood Pressure Response is Eliminated by Alpha 1 Adrenergic Blockade in Human Subjects

IntroductionExposure to traffic-related air pollution is associated with increased risk of cardiovascular disease and mortality. In controlled inhalation studies, exposure to diesel exhaust (DE) has been shown to increase systolic blood pressure (SBP). To examine the hypothesis that DE triggers acute cardiovascular events via neurogenic processes, we investigated the BP response to DE, and whether the effect was modified by an alpha-1 adrenergic receptor antagonist prophylaxis.MethodsTwenty non-smoking, healthy adults, age 18-49 underwent 120-minute controlled exposures to each of 4 conditions [DE (300 μg/m PM2.5) or filtered air (FA), and placebo or terazosin] in a double-blind, placebo-controlled crossover trial. Terazosin (1-2 mg) or matched placebo was administered 2 hours prior to exposures in randomized order. BP was measured before, during (5 times), and after exposure (1h, 3h, 5h, 24h). Baseline-adjusted BP change was compared by subject for each exposure to determine the difference between DE and FA, with and without pretreatment, using mixed effects models to account for the hypotensive effect of terazosin.ResultsCompared with FA, SBP increased 2.4 mmHg (p=0.003) overall, with the peak effect 24h post exposure (6.75 mmHg, p=0.01). Terazosin prophylaxis eliminated the DE effect at all time points. Diastolic BP and heart rate were not modified by DE.ConclusionDE exposure was associated with an increase in SBP during and after inhalation, an effect mitigated by alpha-1 adrenergic receptor blockade. This finding suggests that the short-term vascular effects associated with exposure to traffic-related air pollution occur via autonomic signaling.