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BIOMAKERS OF EXPOSURE AND METABOLIC SUSCEPTIBILITY TO FINE PARTICLE AIR POLLUTION
Citation:
Lewtas, J, B. Binkova, S. R. Myers, J. Lenieek, P. Subrt, AND R. J. Sram. BIOMAKERS OF EXPOSURE AND METABOLIC SUSCEPTIBILITY TO FINE PARTICLE AIR POLLUTION. Presented at ISEA Conference, Monterey, CA, October 24-27, 2000.
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:
The influence of metabolic susceptibility (GSTM1 and NAT2 genotypes) on the association between personal air exposures and biomarkers of exposure, dose, and genetic damage were measured for 60 individuals in two regions exposed to ambient air in the Czech Republic. Personal monitors measured exposure to respirable air particles (<1.7 /um) and the adsorbed polycyclic aromatic hydrocarbons (PAH) for 24 h before collection of blood and urine. Blood samples were analyzed for trace metals, metabolic genotype, DNA adducts, protein adducts, chromosomal aberrations, and sister chromatid exchanges. Urine samples were analyzed for PAH metabolites, cotinine and mutagenic activity. At these environmental exposures to PM1.7 (0.8 -140ug/m3) and PAH (2 - 26 /ng/m3), personal exposures to PM1.7 were significantly correlated with persona] exposures to carcinogenic PAH (r= 0.79, p< 0.0001, n=60), total urinary PAH metabolites (r= 0.48, p= 0.0002, n=58), and two of the trace element levels in blood, selenium (r= 0.55, p< 0.0001, n=60) and lead (r= 0.39, p = 0.003, n=58). DNA adduct levels were significantly and linearly correlated with PAH exposure for the nonsmokers (r=0.36, p<0.05(), n=28) with either GSTMl(r=0.59, p<0.005, n=21) or NAT2 rapid (r=0.47, p<0.057, n=17) genotype present. There was a significant increase in correlation between personal PAH exposure and urinary PAH metabolites for NAT2 slow acetylators (r=0.58, p=0.001) compared to NAT2 rapid and GSTM1 genotypes. This suggests that variations in metabolic genotype account for some of the inter-individual variability observed in human biomarker measurements. The urinary PAH metabolites and trace element levels in blood provide potential source tracers for apportioning the sources of human exposure to fine particles. The selenium was associated with high sulfur coal and lead with the leaded gasoline in use during this study. The individual PAH profile is consistent with the sources of PAH in this region.
This work has been funded by the US Environmental Protection Agency. It has been subjected to Agency review and approved/or publication