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A major route of exposure to hydrophobic organic contaminants (HOCs), such as benzo[a]pyrene (BaP), is ingestion. Matrix-bound HOCs may become bioavailable after mobilization by the gastrointestinal fluids followed by sorption to the intestinal epithelium. The purpose of this research was to measure the bioavailability of [14C]-BaP bound to pristine soils or field-contaminated sediment using an in vitro model of gastrointestinal digestion followed by sorption to human enterocytes (Caco-2 cells) or to a surrogate membrane, ethylene vinyl acetate (EVA) thin film. Although Caco-2 cells had a twofold higher lipid-normalized fugacity capacity than EVA, [14C]-BaP uptake by Caco-2 lipids and EVA thin film demonstrated a linear relationship within the range of BaP concentrations tested. These results suggest that EVA thin film is a good membrane surrogate for passive uptake of BaP. The in vitro system provided enough sensitivity to detect matrix effects on bioavailability; after 5 h, significantly lower concentrations of [14C]-BaP were sorbed into Caco-2 cells from soil containing a higher percentage of organic matter compared to soil with a lower percentage of organic matter. The [14C]-BaP desorption rate from Caco-2 lipids consistently was twofold higher than from EVA thin film for all matrices tested. The more rapid kinetics observed with Caco-2 cells probably were due to the greater surface area available for absorption/desorption in the cells. After 5 h, the uptake of BaP into Caco-2 lipid was similar in live and metabolically inert Caco-2 cells, suggesting that the primary route of BaP uptake is by passive diffusion. Moreover, the driving force for uptake is the fugacity gradient that exists between the gastrointestinal fluid and the membrane.

Accurate estimates for the oral bioavailability of hydrophobic contaminants bound to solid matrices are challenging to obtain because of sorption to organic matter. The purpose of this research was to measure the bioavailability of [14C]chrysene sorbed to soil using an in vitro model of gastrointestinal digestion and absorption to a surrogate intestinal membrane, ethylene vinyl acetate (EVA) thin film. The [14C]chrysene moved rapidly from soil into the aqueous compartment and reached steady state within 2 h. Equilibrium was reached in the EVA film within 32 h. Aging the spiked soil for 6 or 12 months had no effect on chrysene mobilization. This was supported by the finding that the data best fit a one-compartment model. Despite significant decreases in [14C]chrysene mobilization when water or nonneutralized gastrointestinal fluids were used in place of the complete medium, the equilibrium concentration of [14C]chrysene in EVA film remained the same in all conditions. Thus, the driving force for uptake was the fugacity gradient between the aqueous phase and the EVA film. Cultured human enterocytes (human colorectal carcinoma cell line [Caco-2 cells]) had a higher lipid-normalized fugacity capacity than EVA film, but the elimination rate constants were the same, suggesting that the rate was controlled by the resistance of the unstirred aqueous layer at the membrane-water interface.

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