9. Bioaccumulation and Trophic Transfer of Organic Contaminants
221
finding that the contaminant uptake directly from water was by far the fastest
route of accumulation, and that contaminant levels in top trophic levels could
often be produced by bioconcentration alone (LeBlanc, 1995) caused doubt. In
addition, failure to find biomagnification occurring in all ecosystems or in all
components of a food chain was problematic. Highly hydrophobic contaminants
such as PAHs, for instance, do not biomagnify (Bums and Teal, 1979) primarily as
a result of biotransformation. Burrows and Whitton (1983) found that contaminant loads were higher in mayflies than in the predators that ate them. In many
cases, contaminant loads varied randomly between trophic levels without discernible patterns (Biddinger and Gloss, 1984; Kay, 1984; Macek et aI., 1979). In the
absence of a mechanism to account for biomagnification, there was only inconsistent evidence to support its validity.
In a recent review of hundreds of studies on biomagnification, Suedel et al.
(1994) concluded that, although the occurrence ofbiomagnification is much more
limited than previously suggested, it is nonetheless a reality in some systems.
Biomagnification appears to be limited to a small but very important group of
highly lipophilic (log Kow >5), nonmetabolized contaminants that include DDT,
DDE, PCBs, toxaphene, and organic forms of mercury and arsenic. Biomagnification is precluded by, among other things, susceptibility to metabolism and high
elimination rates and can be enhanced when contaminant elimination rates are
slow compared with the energetics of the organism.
9.7.2. A Lipid-Based Model for Biomagnification
Mechanistically, biomagnification appears to consist of a continuation of the same
process that leads to trophic transfer of contaminants. That is, as contaminated
food is digested in the gut, lipids are absorbed and the food volume decreases. The
fugacity of the contaminant in the food, thus, increases above the fugacity of the
chemical in the organism and provides the force necessary to drive the contaminant across the gut by diffusion. The process can be increased by digestion of
nonlipids (e.g., proteins and carbohydrates) because that process increases the
surface area from which sorbed contaminants can be released (DiPinto et aI.,
1993). In addition, it is possible that the compositional changes of partially
digested lipids in the gut will lead to a reduction in fugacity capacity (and increase
in fugacity) without a reduction in food volume (LeBlanc 1995; Gobas et aI.,
1993a).
Although the currently accepted models for both trophic transfer and biomagnification in aquatic systems invoke passive diffusion as the force that transports
contaminants across the GIT into the organism, models derived from terrestrial
mammals have highlighted the possibility that contaminants can also be coassimilated with dietary lipids. In co-assimilation, contaminants move across the
GIT in association with lipids that are being absorbed; the lipids become the
vehicle for contaminant transport. In the second model, the contaminant does not
move by diffusion, because the chemical concentration and fugacity in the organism are similar or higher than levels in the food, but rather via an active process
221
finding that the contaminant uptake directly from water was by far the fastest
route of accumulation, and that contaminant levels in top trophic levels could
often be produced by bioconcentration alone (LeBlanc, 1995) caused doubt. In
addition, failure to find biomagnification occurring in all ecosystems or in all
components of a food chain was problematic. Highly hydrophobic contaminants
such as PAHs, for instance, do not biomagnify (Bums and Teal, 1979) primarily as
a result of biotransformation. Burrows and Whitton (1983) found that contaminant loads were higher in mayflies than in the predators that ate them. In many
cases, contaminant loads varied randomly between trophic levels without discernible patterns (Biddinger and Gloss, 1984; Kay, 1984; Macek et aI., 1979). In the
absence of a mechanism to account for biomagnification, there was only inconsistent evidence to support its validity.
In a recent review of hundreds of studies on biomagnification, Suedel et al.
(1994) concluded that, although the occurrence ofbiomagnification is much more
limited than previously suggested, it is nonetheless a reality in some systems.
Biomagnification appears to be limited to a small but very important group of
highly lipophilic (log Kow >5), nonmetabolized contaminants that include DDT,
DDE, PCBs, toxaphene, and organic forms of mercury and arsenic. Biomagnification is precluded by, among other things, susceptibility to metabolism and high
elimination rates and can be enhanced when contaminant elimination rates are
slow compared with the energetics of the organism.
9.7.2. A Lipid-Based Model for Biomagnification
Mechanistically, biomagnification appears to consist of a continuation of the same
process that leads to trophic transfer of contaminants. That is, as contaminated
food is digested in the gut, lipids are absorbed and the food volume decreases. The
fugacity of the contaminant in the food, thus, increases above the fugacity of the
chemical in the organism and provides the force necessary to drive the contaminant across the gut by diffusion. The process can be increased by digestion of
nonlipids (e.g., proteins and carbohydrates) because that process increases the
surface area from which sorbed contaminants can be released (DiPinto et aI.,
1993). In addition, it is possible that the compositional changes of partially
digested lipids in the gut will lead to a reduction in fugacity capacity (and increase
in fugacity) without a reduction in food volume (LeBlanc 1995; Gobas et aI.,
1993a).
Although the currently accepted models for both trophic transfer and biomagnification in aquatic systems invoke passive diffusion as the force that transports
contaminants across the GIT into the organism, models derived from terrestrial
mammals have highlighted the possibility that contaminants can also be coassimilated with dietary lipids. In co-assimilation, contaminants move across the
GIT in association with lipids that are being absorbed; the lipids become the
vehicle for contaminant transport. In the second model, the contaminant does not
move by diffusion, because the chemical concentration and fugacity in the organism are similar or higher than levels in the food, but rather via an active process