Modeling polycyclic aromatic hydrocarbon bioaccumulation and metabolism in time‐variable early life‐stage exposures

Abstract

Recent laboratory investigations into the bioaccumulation and toxicity of polycyclic aromatic hydrocarbons (PAH) have focused on low-level, time-variable exposures to early life-stage fish. Polycyclic aromatic hydrocarbon body-burden residues reported in these studies were lower than critical body-burden residues predicted by the target lipid model (TLM). To understand this discrepancy, a time-variable uptake and depuration model of PAH bioaccumulation was developed. Kinetic constants were fit using measured exposure and tissue concentrations. The resulting lipid-water partition coefficients (K(LW)) were uncorrelated with the octanol-water partition coefficient (K(OW))--a qualitatively unrealistic finding considering that numerous studies have reported a positive correlation between the two. Because PAHs are known to be metabolized, the comparison of K(LW) with K(OW) suggests that metabolism may be occurring in early life-stage fish. Therefore, the uptake and depuration model was modified to include metabolism while assuming linearity of K(LW) with K(OW). Calculated metabolism rates were positively correlated with K(OW)--a finding qualitatively similar to those of other studies. The present study provides a reasonable explanation for the discrepancy between the TLM predictions and the measured toxic effect levels. Given the time-variable exposure concentrations, the maximum measured body burdens used to relate to toxic effects may be underestimated. In addition, the maximum body burden of parent PAH plus metabolites may be a better measure in relating tissue concentrations to toxic effects. Incorporating these refinements in relating body burdens to toxic effects may result in a better comparison between TLM predictions and measured effect levels.