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Attribution of Particle Exposure and Risk to Combustion Source Emissions Based on Personal PAH Exposure and Urinary Metabolites

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Abstract: Personal airborne exposures to carcinogenic particulate PAH have been significantly correlated with exposure to respirable fine particle mass (PM 2.5) in several studies. All combustion sources emit PAH, however the relative concentrations of different PAH and other organic tracers (source profiles) vary by source category. The underlying hypothesis of this study is that PAH profiles of personal exposure and urinary PAH metabolites are tracers of exposure to different sources of combustion particles. The study objective was to determine the relative contribution of combustion sources to a population through application of positive matrix factorization (PMF) to personal exposure and urinary metabolite data. This approach does not rely on pre-determined source profiles. PMF, was applied to multiple measures of personal exposure including particulate PAH and urinary PAH metabolites. Other measures of personal exposure (e.g., cotinine and blood metals) and metabolic susceptibility (metabolic genotype) were also considered. Personal air filters (PM2.5) were collected for the 24 hours. Urine was collected as a morning void after 24h sampling (Czech Study) or during sampling (Seattle). The personal air filters and urine extracts were analyzed for organic tracers using both HPLC and GC/MS. The urine was treated by enzymatic hydrolysis using b-glucuronidase and arylsulfatase prior to analysis. Data from two human exposure studies were used in this initial analysis including two populations in the Czech Republic where the dominant exposure sources included coal combustion and three susceptible populations in Seattle, WA where the dominant combustion sources included motor vehicles and vegetative burning. Potential source tracers and their metabolites included benzo(ghi)perylene (BghiP), identified as a source tracer for gasoline engine exhaust, methylated PAH associated with coal combustion, the nicotine metabolite, cotinine, as a marker of exposure to tobacco smoke, and specific vegetative burning metabolites (e.g., methoxyphenols) as well as metabolites of the more carcinogenic PAH, such as benzo(a)pyrene (BaP). Initial PMF factor analysis using personal PAH exposure, urine metabolites and blood metals in the Czech population identified three sources of exposure including coal related outdoor air, an indoor tobacco source, and a possible dietary source related to blood metals. Recent PMF analysis of outdoor air measurements in Seattle (1996-1999) resulted in identifying eight sources of PM2.5. Vegetative burning (33.8%), diesel (14.5%), and gasoline vehicles (5.4%) accounted for 54% of the PM2.5. Previous studies linking the outdoor apportionment of combustion sources with the relative tumor-initiating potency of motor vehicle emissions and wood stove (vegetative) burning emissions resulted in a higher relative risk from the motor vehicle emissions.

This work has been funded by the U S Environmental Protection Agency. It has been subjected to Agency review and approved for publication.
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Citation:Lewtas, J., S. Meyers, N. Maykut, C. Simpson, D. Kalman, L. S. Liu, and T. V. Larson. Attribution of Particle Exposure and Risk to Combustion Source Emissions Based on Personal PAH Exposure and Urinary Metabolites. Presented at International Society of Exposure Analysis, Vancouver, Canada, August 11-15, 2002.
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Contact: Liz Hope - (919) 541-2785 or hope.elizabeth@epa.gov
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Division: Human Exposure & Atmospheric Sciences Division
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Branch: Immediate Office
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Product Type: Abstrct/Oral
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Presented: 08/11/2002
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Related Entries:
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Bullet Item Biomarkers of PM Exposure to Combustion Source Emissions & Organic (Toxic) Components
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