Student Research: Kristen Cosselman

, Environmental Toxicology (Tox), 2011
Faculty Advisor: Joel D. Kaufman

Traffic-Related Air Pollution: Science and Policy: Blood Pressure Response to Controlled Diesel Exhaust Exposure in Human Subjects & Factors Influencing Air Quality Policy Implementation and Success


Abstract

Recent research has demonstrated that exposure to fine particulate matter (PM2.5), a component of traffic-related air pollution, is associated with increased risk of cardiac ischemia, arrhythmia, and increased circulating markers of inflammation and thrombosis. Though the underlying mechanisms remain unclear, it has been proposed that pulmonary deposition of PM2.5 may trigger an autonomic nervous system imbalance, leading to a rapid increase in blood pressure (BP). To investigate mechanisms through which inhaled PM2.5 potentiates cardiovascular events, we examined BP response in human subjects exposed to inhaled diesel exhaust (DE), a dominant source of urban PM2.5. We further examined whether BP response varied by genotype for the angiotensin II type 1 receptor (AGTR1) single nucleotide polymorphism A1166C (rs5186). AGTR1 is a key modulator of the vascular effects of angiotensin II and has been found to play a significant role in cardiovascular risk associated with increased BP.

Subjects included fifty-two adult non-smokers, age 18-49; thirty-five healthy and seventeen with metabolic syndrome. Exposures were double-blind, crossover, and randomized to order, with sessions separated by a minimum two-week washout period. Each subject was exposed to each condition, 200 μg/m3 DE or filtered air, for a duration of 120 minutes. Blood pressure was measured using an automated oscillometric monitor. Baseline vitals were taken upon subject arrival, at thirty-minute intervals during exposure, and at one, two and four hours post exposure. Subjects returned the following morning for follow up BP measurements.

Preliminary analyses of pair-wise differences by subject at each time point show positive mean effects of DE exposure on systolic blood pressure, with females demonstrating a consistently stronger, but not significant, response at all time points. Further analysis will include paired t-tests, mixed model effects, and ANOVA. Differences in difference within and across exposures will be compared, adjusting for session order, age, gender, BMI, cholesterol level and AGTR1 genotype.