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Cardiovascular Effects Caused by Increasing Concentrations of Diesel Exhaust in Middle-Aged Healthy GSTM1 Null Human Volunteers
Citation:
Tong, H., A. Rappold, M. Caughey, A. Hinderliter, D. Graff, J. Berntsen, W. Cascio, R. Devlin, AND J. Samet. Cardiovascular Effects Caused by Increasing Concentrations of Diesel Exhaust in Middle-Aged Healthy GSTM1 Null Human Volunteers. INHALATION TOXICOLOGY. Taylor & Francis, Inc., Philadelphia, PA, 26(6):319-326, (2014).
Impact/Purpose:
This study examined the cardiovascular effects from increasing concentrations of diesel exhaust in healthy middle-aged human volunteer.
Description:
ABSTRACT Objectives: Epidemiological studies have shown an association between the incidence of adverse cardiovascular effects and exposure to ambient particulate matter (PM). Diesel exhaust (DE) is a major contributor to ambient PM in urban areas. This study was designed to evaluate the concentration responses of short-term exposure to DE on the cardiovascular system. Methods: Six healthy middle-aged participants with GSTM1 null genotype underwent three 2 hr-exposures to three different concentrations of DE sampled in real time from the exhaust of an idling diesel truck engine. The three DE concentrations were 100 µg/m3, 200 µg/m3, and 300 µg/m3 and were conducted at least 14 days apart. Results: We demonstrated that the cardiovascular effects of DE exposure were concentration-dependent. We report that lowest concentration of DE exposure caused minimal cardiovascular effects, while exposure to 300 µg/m3 DE resulted in a statistically significant reduction of baseline brachial artery diameter (BAD) (3.34±0.27 mm pre- vs. 3.23±0.25 mm post-exposure; p<0.05). Diastolic blood pressure was increased by 5 mmHg and the frequency domain of HRV decreased after inhalation of 300 µg/m3 DE in middle-aged GSTM1 null participants. Conclusion: These findings demonstrate that relatively high concentrations of DE are needed to observe robust cardiovascular changes in humans acutely exposed to this pollutant. This study suggests that arterial vasoconstriction and HRV alteration may be one mechanism by which traffic-related air pollution contributes to cardiovascular risk.