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13 EFFECTS OF DIESEL EXHAUST EXPOSURE ON C-REACTIVE PROTEIN AND SERUM AMYLOID A
  1. K. Gemar,
  2. J. Sullivan,
  3. J. Kaufman
  1. University of Washington, Seattle, 1McGill University and KSDPP, University of Washington School of Medicine

Abstract

Background Increases in fine particulate air pollution (PM 2.5) have been linked to rises in cardiovascular hospital admissions and deaths. Yet, the mechanism behind this effect remains unknown. C-Reactive Protein (CRP) and Serum Amyloid A (SAA) are inflammatory markers produced by the liver in response to IL-6 that are thought to be of value for predicting cardiovascular events. Studies have linked PM2.5 exposure to a rise in inflammatory markers including SAA and CRP in the blood, but have always relied on estimating incidental PM2.5 exposure. We hypothesized that exposure to 200 μg/m3 diesel exhaust particles (DEP) for two hours would result in a rise in inflammatory markers at a sampling time 22 hours after the beginning of the exposure in young healthy adults

Study Design and Methods We proposed a randomized crossover experiment in nine healthy individuals to four exposure conditions (filtered air or diesel exhaust at 50, 100, or 200 μg DEP PM2.5 /m3). Subjects were exposed in a 100 cubic meter exposure chamber. Exposure was characterized using continuous reading instruments (TEOM, PSAP, 2 CPCs, CO monitor, and NOx monitor). Blood samples were collected before exposure, as well as 6 hours and 22 hours after the onset of the exposure session. High-sensitivity CRP and SAA assays were run on each of the samples.

Results Changes were seen in CRP levels following exposure to diesel exhaust when compared with the control exposure, but because of the small sample size, the results cannot be considered significant. For the eight subjects with complete data, six had an increase in CRP at 22 hours following the 200 μg/m3 exposure that ranged from 0.2 to 2.0 mg/L, with one subject remaining unchanged and another showing a decrease in CRP concentration. For the four subjects with complete SAA data, no consistent relationship was appreciated. Data from this pilot study helped us to see that changes, especially in CRP, do appear to occur at the chosen sampling times and the protocol is encouraging for a larger study.

Conclusion A continuation of this study with a larger sample size would be valuable in determining whether a rise in the studied inflammatory markers occurs in response to controlled exposure to diesel exhaust.

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