9. Bioaccumulation and Trophic Transfer of Organic Contaminants
225
passed to embryos via the egg (Burger and Gochfeld, 1993; Jarman et aI., 1993;
Heinz et aI., 1989). In some cases, the concentrations of contaminants in eggs
exceed the concentrations found in parental tissues (Heinz, 1993; Tillitt et aI.,
1992). Similar results have been obtained for reptiles (e.g., snapping turtles, in
which lipid storage of contaminants in adult adipose tissue often protects the adult
turtle from overt symptoms of poisoning). However, liberal transfer of maternal
residues to eggs has been documented several times (Loganathan et aI., 1995;
Bishop et aI., 1994; Struger et aI., 1993). Physiological effects in contaminated
embryos of both birds and reptiles such as depressions in the titers of key hormones (e.g., estradiol or enzymes) (Chen et aI., 1994; Trust et aI., 1994), gross
structural abnormalities (Hansen, 1994), embryo death, and complete reproductive failure (van den Berg et aI., 1994; Bishop et aI., 1991) have been attributed to
transgenerational transfer of contaminant loads.
Although reproductive processes are infrequently studied with contaminant
fate as a focus, it is clear from what is known of reproductive physiology that lipid
metabolism is likely to playa key role in trans generational contaminant transfer.
In birds, reptiles, amphibians, and fish, developing oocytes take up large amounts
of maternally derived vitellogenin, which consists of about 20% lipid, to serve as
an energy source during subsequent development. In addition, lipids are also
taken up directly from maternal stores or synthesized de novo by the embryo from
maternal extrahepatic lipid (Mommen and Walsh, 1988). The development of the
embryo can be reasonably viewed as taking place in a lipid-rich environment. If
the maternal lipids are contaminated, then transfer of the contaminants to the
embryo could easily take place following the normal pathways of lipid deposition
in the embryo during reproduction. Further, because the lipid content of the
embryo is high, relative to maternal tissues, the increase in lipid content will
increase the fugacity capacity of the embryo, decrease its fugacity (for a given
concentration, increasing Z decreases j), and increase the tendency of the contaminant to move into the embryo. That is, a mechanism for explaining observed
"reproductive magnification" of residues in embryonic tissues exists and relates
directly to lipid content.
The above scenario is largely unstudied but presents several testable hypotheses that could serve as the focus for additional research. For instance, maternal
contaminant loads (lipid normalized) should decrease after a brood has been
produced if maternal lipid reserves are the source of embryonic contamination.
There is at least one report confirming this assertion in fish (Sijm et aI., 1992), but
data in other species are needed. In addition, the hypothesis suggests that residues
in embryos should increase in proportion to the lipid content of the embryo.
Monitoring those changes throughout larval development should be informative.
In any event, the primacy of lipid levels in determining all aspects of contaminant
uptake highlights the need to examine its role in reproduction because the biological impacts on reproduction appear to be detrimental.
225
passed to embryos via the egg (Burger and Gochfeld, 1993; Jarman et aI., 1993;
Heinz et aI., 1989). In some cases, the concentrations of contaminants in eggs
exceed the concentrations found in parental tissues (Heinz, 1993; Tillitt et aI.,
1992). Similar results have been obtained for reptiles (e.g., snapping turtles, in
which lipid storage of contaminants in adult adipose tissue often protects the adult
turtle from overt symptoms of poisoning). However, liberal transfer of maternal
residues to eggs has been documented several times (Loganathan et aI., 1995;
Bishop et aI., 1994; Struger et aI., 1993). Physiological effects in contaminated
embryos of both birds and reptiles such as depressions in the titers of key hormones (e.g., estradiol or enzymes) (Chen et aI., 1994; Trust et aI., 1994), gross
structural abnormalities (Hansen, 1994), embryo death, and complete reproductive failure (van den Berg et aI., 1994; Bishop et aI., 1991) have been attributed to
transgenerational transfer of contaminant loads.
Although reproductive processes are infrequently studied with contaminant
fate as a focus, it is clear from what is known of reproductive physiology that lipid
metabolism is likely to playa key role in trans generational contaminant transfer.
In birds, reptiles, amphibians, and fish, developing oocytes take up large amounts
of maternally derived vitellogenin, which consists of about 20% lipid, to serve as
an energy source during subsequent development. In addition, lipids are also
taken up directly from maternal stores or synthesized de novo by the embryo from
maternal extrahepatic lipid (Mommen and Walsh, 1988). The development of the
embryo can be reasonably viewed as taking place in a lipid-rich environment. If
the maternal lipids are contaminated, then transfer of the contaminants to the
embryo could easily take place following the normal pathways of lipid deposition
in the embryo during reproduction. Further, because the lipid content of the
embryo is high, relative to maternal tissues, the increase in lipid content will
increase the fugacity capacity of the embryo, decrease its fugacity (for a given
concentration, increasing Z decreases j), and increase the tendency of the contaminant to move into the embryo. That is, a mechanism for explaining observed
"reproductive magnification" of residues in embryonic tissues exists and relates
directly to lipid content.
The above scenario is largely unstudied but presents several testable hypotheses that could serve as the focus for additional research. For instance, maternal
contaminant loads (lipid normalized) should decrease after a brood has been
produced if maternal lipid reserves are the source of embryonic contamination.
There is at least one report confirming this assertion in fish (Sijm et aI., 1992), but
data in other species are needed. In addition, the hypothesis suggests that residues
in embryos should increase in proportion to the lipid content of the embryo.
Monitoring those changes throughout larval development should be informative.
In any event, the primacy of lipid levels in determining all aspects of contaminant
uptake highlights the need to examine its role in reproduction because the biological impacts on reproduction appear to be detrimental.