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EVALUATION OF URINARY PAH METABOLITES AS BIOMARKERS OF EXPOSURE TO PM2.5 FROM COMBUSTION SOURCES
Citation:
Lewtas, J, S. Myers, C. Simpson, D. Kalman, AND S. Liu. EVALUATION OF URINARY PAH METABOLITES AS BIOMARKERS OF EXPOSURE TO PM2.5 FROM COMBUSTION SOURCES. Presented at International Symposium on Polycyclic Aromatic Compounds, Amsterdam, The Netherlands, September 21-25, 2003.
Impact/Purpose:
The objective of this task is to develop and evaluate personal exposure and biomarker methods for toxic components associated with PM2.5 and SVOC in population exposures. Specific sub-objectives include the following:
1) Identification and quantification of either toxic or tracer organic chemicals associated with PM2.5 and associated SVOC.
2) Measurement of personal airborne exposure of selected toxic/tracer organic species in population based human exposure studies.
3) Development and application of urinary metabolite and other biomarker methods for these toxic/tracer organic species in human exposure studies.
4) Evaluation of multivariant receptor models for apportioning personal exposure using biomarker data.
Description:
This study determined the relationship between daily personal exposure to airborne fine particles (PM2.5) and the excretion of urinary PAH metabolites over a 10-day period of repeated measurements. The samples (n=60) were selected from a large series of exposure and health panel studies conducted in Seattle (Liu et al. Env. Health Perspectives, 2003). The sample sets were selected to represent the maximum observed variation in personal exposures over the 10-day panel study period. The PAH metabolites (n = 27) were analyzed by GC/MS/SIM and HPLC/fluorescence. Personal exposures to PM2.5 mass varied from 1.6-66.6 ug/m3 (16.4 mean) and the personal PAH exposures varied from 3.5-14.3 ng/m3 (7.0 mean). Exposures to the wood smoke marker, levoglucosan, ranged from 0.6- 490 ng/m3 (47.5 mean). Outdoor PM2.5 was highly correlated (P < 0.001) with the personal exposures to PM2.5, PAH, and levoglucosan. The urinary PAH metabolites exhibited less variation over the 10 days sampled (1.5-3 fold) than found in the personal exposures. No significant correlation was found between exposure measures and urinary biomarkers within the 10-day period. Although we were not able to determine the half-life, the results are consistent with metabolites (e.g., cotinine) with a relatively long half-life. Previous studies of the half-lives (t 1/2) for urinary elimination of several PAH show evidence of two-phase elimination with a short t 1/2 (4-8h) and a long t 1/2 (12-20h). This study is compared to a study in the Czech Republic where higher personal exposures to PAH were observed than in Seattle and the study was conducted at one time period with 60 subjects. In the Czech study, urinary PAH metabolites were significantly correlated with personal PM2.5 and PAH. These results are also consistent with the longer half-life for urinary PAH metabolites. The use of urinary metabolites and other biomarkers are being explored as tools to apportion human population exposures to PM2.5 from different combustion source emissions.
This work has been funded by the United States Environmental Protection Agency. This work has been subjected to Agency review and approved for publication.