224
p.F. Landrum and S.w. Fisher
Although the arguments against biomagnification cited above are compelling,
there are some situations in which accumulation of a contaminant in an organism
above residues found in its food cannot be explained in any way other than
biomagnification. For instance, Rasmussen et al. (1990) compared PCB concentrations in a single predatory fish species, lake trout (Salvelinus namaycush)
from more than 80 different sites throughout Ontario. Despite the fact that the lake
trout in all sites experienced similar environmental exposure levels to PCBs, the
actual concentrations of PCBs in lake trout varied from IS to 10,000 ppb. The
between-lake variation in PCB content in lake trout was attributed to two factors:
length of the food chain and increase in lipid levels as a function of food chain
length. Each trophic link in the food chain resulted in a magnification of PCB
concentrations by a factor of approximately 3-5. Thus, when the length of the
food chain was relatively short, the lake trout were much less contaminated than
when the food chain was longer. Lipid levels also increased with food chain
length. However, lipid levels increased by a factor of 1.5 with each trophic link
and cannot, therefore, account for the magnification of PCBs at each step. In other
words, biomagnification of PCB residues from food must be occurring (Rowan
and Rasmussen, 1992). A trophic position model for lake trout has been developed for both PCB and mercury biomagnification (Vanderzanden and Rasmussen, 1996). Similarly, biomagnification was found to account for high Kow
PCB congeners in white bass (Morone chysops) in the Lake Erie food web based
on a fugacity analysis (Russell et aI., 1995) and in fresh water, Lake Nieuwe Meer,
in The Netherlands (van der Oost et aI., 1988). Further, the presumed increase in
total lipid content with each trophic step does not always occur while biomagnification is observed (Broman et aI., 1992), thus refuting the arguments that it is
increases in lipid content driving the presumed biomagnification put forth by
LeBlanc (1995). In situ biomagnification has been difficult to demonstrate, in part
because of the difficulty in placing organisms at appropriate levels within a food
chain. However, with the use of stable isotope analysis, the biomagnification of
polychlorinated dibenzodioxins and polychlorinated dibenzofurans was clearly
demonstrated for a Baltic Sea food chain (Broman et aI., 1992).
In short, the relative contributions of contaminated food versus contaminated
media may vary between ecosystems or even between organisms within an ecosystem. However, residue data suggest that biomagnification of specific contaminants occurs in nature. This, combined with knowledge of a mechanism for
understanding of the process of biomagnification and data that show magnification of residues from food when other avenues of contaminant exposure are
precluded, provides strong support for the validity of biomagnification.
9.8. Lipids and Transgenerational Transfer of Contaminants
Loss of stored contaminant residues in female animals through reproduction is
now understood as a key elimination mechanism, particularly in long-lived species (Sijm et aI., 1992). For instance, contaminant residues in adult birds may be
p.F. Landrum and S.w. Fisher
Although the arguments against biomagnification cited above are compelling,
there are some situations in which accumulation of a contaminant in an organism
above residues found in its food cannot be explained in any way other than
biomagnification. For instance, Rasmussen et al. (1990) compared PCB concentrations in a single predatory fish species, lake trout (Salvelinus namaycush)
from more than 80 different sites throughout Ontario. Despite the fact that the lake
trout in all sites experienced similar environmental exposure levels to PCBs, the
actual concentrations of PCBs in lake trout varied from IS to 10,000 ppb. The
between-lake variation in PCB content in lake trout was attributed to two factors:
length of the food chain and increase in lipid levels as a function of food chain
length. Each trophic link in the food chain resulted in a magnification of PCB
concentrations by a factor of approximately 3-5. Thus, when the length of the
food chain was relatively short, the lake trout were much less contaminated than
when the food chain was longer. Lipid levels also increased with food chain
length. However, lipid levels increased by a factor of 1.5 with each trophic link
and cannot, therefore, account for the magnification of PCBs at each step. In other
words, biomagnification of PCB residues from food must be occurring (Rowan
and Rasmussen, 1992). A trophic position model for lake trout has been developed for both PCB and mercury biomagnification (Vanderzanden and Rasmussen, 1996). Similarly, biomagnification was found to account for high Kow
PCB congeners in white bass (Morone chysops) in the Lake Erie food web based
on a fugacity analysis (Russell et aI., 1995) and in fresh water, Lake Nieuwe Meer,
in The Netherlands (van der Oost et aI., 1988). Further, the presumed increase in
total lipid content with each trophic step does not always occur while biomagnification is observed (Broman et aI., 1992), thus refuting the arguments that it is
increases in lipid content driving the presumed biomagnification put forth by
LeBlanc (1995). In situ biomagnification has been difficult to demonstrate, in part
because of the difficulty in placing organisms at appropriate levels within a food
chain. However, with the use of stable isotope analysis, the biomagnification of
polychlorinated dibenzodioxins and polychlorinated dibenzofurans was clearly
demonstrated for a Baltic Sea food chain (Broman et aI., 1992).
In short, the relative contributions of contaminated food versus contaminated
media may vary between ecosystems or even between organisms within an ecosystem. However, residue data suggest that biomagnification of specific contaminants occurs in nature. This, combined with knowledge of a mechanism for
understanding of the process of biomagnification and data that show magnification of residues from food when other avenues of contaminant exposure are
precluded, provides strong support for the validity of biomagnification.
9.8. Lipids and Transgenerational Transfer of Contaminants
Loss of stored contaminant residues in female animals through reproduction is
now understood as a key elimination mechanism, particularly in long-lived species (Sijm et aI., 1992). For instance, contaminant residues in adult birds may be