You are here:
CONTROLLED EXPOSURES OF HUMAN VOLUNTEERS TO DIESEL ENGINE EXHAUST: BIOMARKERS OF EXPOSURE AND HEALTH OUTCOMES
Citation:
Madden, M., T. Stevens, M. Case, J. Sobus, M. Stiegel, D. Diaz-Sanchez, W. Cascio, R. Devlin, AND J. Pleil. CONTROLLED EXPOSURES OF HUMAN VOLUNTEERS TO DIESEL ENGINE EXHAUST: BIOMARKERS OF EXPOSURE AND HEALTH OUTCOMES. Presented at International Society for Aerosols in Medicine (ISAM), April 06 - 10, 2013.
Impact/Purpose:
This is an abstract of a proposed presentation at a local meeting to primarily aerosol scientists and is not intended to represent official US EPA policy. The invited presentation is intended to inform the audience about biological responses and exposure estimates to diesel exhaust exposures in controlled settings and is part of a larger symposium on health effects from diesel exhaust.
Description:
Combustion of diesel fuel contributes to ambient air pollutant fine particulate matter (PM) and gases. Fine PM exposure has been associated with increased mortality due to adverse cardiac events, and morbidity, such as increased hospitalization for asthma symptoms and lung infections. Controlled exposure studies with diesel exhaust (DE) have been used, in part, to examine if epidemiological observations between PM exposure and health effects had biological plausibility. In our facility, exposures of healthy, adolescent human volunteers were exposed to either 100 ug/m3 DE to identify markers of exposure and effect. At 100 ug/m3 exposure, small changes in plasma cytokine and clotting factors were observed without lung function changes. Urinary naphthalene and phenanthrene appear to surrogates of the exposure. For 300 ug/m3 DE exposures, we examined lung function effects with both concurrent and sequential 300 ppb ozone (O3) exposure. Subjects received either air FA, O3, DE, or DE+O3 on Day 1, followed by only O3 exposures on Day 2. Exposures were for 2 hr with intermittent, moderate exercise. For lung function on Day 1, FA and DE did not induce FEV1 changes, O3 decreased FEV1 16+3%, while DE+O3 decreased FEV1 22+4%. On Day 2 after the O3 challenge, subjects who were exposed to DE on Day 1 had a greater FEV1 decrement (18+4%) compared to the FEV1 decrements of subjects (11+3%) receiving air exposure on Day 1. Lung function recovered to approximately pre-exposure values within 4 hr at similar rates in all groups on both Days 1 and 2. These data suggest that simultaneous DE+O3 exposure can synergistically decrease FEV1, and sequential DE followed by O3 exposures can induce a greater FEV1 decrement than FA/O3 exposures. Disclaimer: This is an abstract of a proposed presentation and may not represent official US EPA policy. Funding by US EPA; Protocols approved by the UNC Biomedical IRB.