Characterization of EPA's 16 priority pollutant polycyclic aromatic hydrocarbons (PAHs) in tank bottom solids and associated contaminated soils at oil exploration and production sites in Texas.

The purpose of this study was to determine the concentration and types of polycyclic aromatic hydrocarbons (PAHs), a group of environmentally toxic and persistent chemicals, at contaminated oil exploration and production (E&P) sites located in environmentally sensitive and geographically distinct areas throughout Texas. Samples of tank bottom solids, the oily sediment that collects at the bottom of the tanks, were collected from inactive crude oil storage tanks at E&P sites and hydrocarbon contaminated soil samples were collected from the area surrounding each tank that was sampled. All samples were analyzed for the 16 PAH priority pollutant listed by US EPA and for total petroleum hydrocarbons (TPH). The results demonstrate that overall average PAH concentrations were significantly higher in tank bottom solids than in contaminated soils. Total PAH concentrations decreased predictably with diminishing hydrocarbon concentrations; but the percent fraction of carcinogenic PAHs per total measured PAH content increased from approximately 12% in tank bottom solids to about 46% in the contaminated soils. These results suggest that the PAH content found in tank bottom solids cannot reliably be used to predict the PAH content in associated contaminated soil. Comparison of PAHs to conservative risk-based screening levels for direct exposure to soil and leaching from soil to groundwater indicate that PAHs are not likely to exceed default risk-based thresholds in soils containing TPH of 1% (10,000mg/kg) or less. These results show that the magnitude of TPH concentration may be a useful indicator of potential risk from PAHs in crude oil-contaminated soils. The results also provide credibility to the 1% (10,000mg/kg) TPH cleanup level, used in Texas as a default management level at E&P sites located in non-sensitive areas, with respect to PAH toxicity.