218
P.F. Landrum and S.W. Fisher
to correct for variability in accumulation due to lipid content. This model works
well but is very dependent on the concentrations in the lower food web that are
predicted from equilibrium partitioning theory (Thomann, 1989).
9.6.2.2. Mechanism for Trophic Transfer
The fugacity-based approach to understanding trophic transfer has yielded important information about the mechanisms of trophic transfer and their relationship to
lipid levels. One implication of the fugacity model, for instance, is that the
fugacity of the food must be higher than the fugacity of the organism for trophic
transfer to occur. This can occur if the predator is kinetically limited in achieving
steady state compared with the prey. Then the prey will be at a higher thermodynamic chemical potential than the predator. Such a situation can easily occur
with large growing predators such as large fish that may never attain the thermodynamic chemical potential of the system, and thus transfer of the contaminant
will continue down a chemical activity gradient. It may also be the case that the
prey is exposed to sources not available to the predator (e.g., the prey come from
the sediment and the predator only experiences the overlying water). This could
readily occur because fine sediments are focused into depositional areas that are
often out of thermodynamic equilibrium with the overlying water.
More often, however, the predator and prey may be at the same thermodynamic
potential relative to the major source (e.g., water). How then can bioaccumulation
occur from the prey to the predator? By empirical observation, most organisms in
a food web appear to have similar fugacities (Gobas et aI., 1993a). Thus, the
required lipid-water-lipid partition (chemical activity gradient) that is needed to
move a contaminant from ingested food into an aqueous phase and then back to a
lipid phase in the organism would seem to be absent. Thus, if trophic transfer were
to occur, contaminants would have to move without or against a fugacity gradient.
In the absence of active uptake, there is no mechanism to account for this.
A focus on lipid and its influence on contaminant transfer has been invoked to
explain this apparent contradiction. When contaminated food is ingested by an
organism, the contaminants move into the gastrointestinal tract (GIT) in association with lipids. Once present in the gut, digestion begins to take place. Lipids are
dissociated from the bulk of ingested material, acted on by specific enzymes, and
transported across the gut wall via specific lipoprotein carriers. Two hypotheses
can be invoked for contaminant transfer: ( 1) the contaminants may stay associated
with the lipid material and move with the lipids actively, and (2) the contaminants
are left behind while the lipids are digested and absorbed. This has two important
consequences: (I) there is a smaller food volume remaining in the gut, resulting in
a momentary increase in the contaminant concentration; and (2) the food remaining in the GIT has lost part of the lipid component that sequesters contaminants.
Thus, the ability of the remaining food to dissolve the contaminant is reduced and
the fugacity capacity of the food goes down, causing the fugacity of the food to
become higher than that of the organism. The increase in concentration and
fugacity of the contaminant in the food relative to the organism causes the contaminants to passively diffuse food across the gut wall into the organism. Thus,
P.F. Landrum and S.W. Fisher
to correct for variability in accumulation due to lipid content. This model works
well but is very dependent on the concentrations in the lower food web that are
predicted from equilibrium partitioning theory (Thomann, 1989).
9.6.2.2. Mechanism for Trophic Transfer
The fugacity-based approach to understanding trophic transfer has yielded important information about the mechanisms of trophic transfer and their relationship to
lipid levels. One implication of the fugacity model, for instance, is that the
fugacity of the food must be higher than the fugacity of the organism for trophic
transfer to occur. This can occur if the predator is kinetically limited in achieving
steady state compared with the prey. Then the prey will be at a higher thermodynamic chemical potential than the predator. Such a situation can easily occur
with large growing predators such as large fish that may never attain the thermodynamic chemical potential of the system, and thus transfer of the contaminant
will continue down a chemical activity gradient. It may also be the case that the
prey is exposed to sources not available to the predator (e.g., the prey come from
the sediment and the predator only experiences the overlying water). This could
readily occur because fine sediments are focused into depositional areas that are
often out of thermodynamic equilibrium with the overlying water.
More often, however, the predator and prey may be at the same thermodynamic
potential relative to the major source (e.g., water). How then can bioaccumulation
occur from the prey to the predator? By empirical observation, most organisms in
a food web appear to have similar fugacities (Gobas et aI., 1993a). Thus, the
required lipid-water-lipid partition (chemical activity gradient) that is needed to
move a contaminant from ingested food into an aqueous phase and then back to a
lipid phase in the organism would seem to be absent. Thus, if trophic transfer were
to occur, contaminants would have to move without or against a fugacity gradient.
In the absence of active uptake, there is no mechanism to account for this.
A focus on lipid and its influence on contaminant transfer has been invoked to
explain this apparent contradiction. When contaminated food is ingested by an
organism, the contaminants move into the gastrointestinal tract (GIT) in association with lipids. Once present in the gut, digestion begins to take place. Lipids are
dissociated from the bulk of ingested material, acted on by specific enzymes, and
transported across the gut wall via specific lipoprotein carriers. Two hypotheses
can be invoked for contaminant transfer: ( 1) the contaminants may stay associated
with the lipid material and move with the lipids actively, and (2) the contaminants
are left behind while the lipids are digested and absorbed. This has two important
consequences: (I) there is a smaller food volume remaining in the gut, resulting in
a momentary increase in the contaminant concentration; and (2) the food remaining in the GIT has lost part of the lipid component that sequesters contaminants.
Thus, the ability of the remaining food to dissolve the contaminant is reduced and
the fugacity capacity of the food goes down, causing the fugacity of the food to
become higher than that of the organism. The increase in concentration and
fugacity of the contaminant in the food relative to the organism causes the contaminants to passively diffuse food across the gut wall into the organism. Thus,