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

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.