CHAPTER 13 • Mercury in Marine Environments
13.6
Mercury in the Marine Food Chain
13.6.1
Bioaccumulation
255
The production of methyl mercury in aquatic systems is the first stage in the aquatic
bioaccumulation process (WHO/IPCS 1990). Bioaccumulation is distinct from
biomagnification (Mance 1987). Bioaccumulation involves the uptake from water independently by each trophic level and species, whereas biomagnification involves the
transfer from one trophic level to another by ingestion. Forstner and Wittmann (1979)
concluded that because of its high affinity for organic substances, mercury (together
with arsenic) was likely to show biomagnification of the food chain. There is, however, conflicting evidence in the literature. Some studies have reported an increase along
the food chain (e.g. Knauer and Martin 1972), whereas others have shown no consistent increase (e.g. Leatherland and Burton 1975). It has been shown, however, that Hgr
concentrations and the percentage of methyl mercury increase in older organisms and
those at the top of the food chain (Bernhard 1985, 1988). It was suggested, from models, that this is brought about because the inorganic mercury reaches a constant concentration early in the lifespan, while that for methyl mercury increases with the size
of the specimen and the trophic level of the species.
Minganti et al. (1996) studied the accumulation of mercury along the web of seafood species in the Ligurian Sea. They investigated five crustaceans, whose trophic
positions in the food web from herbivore/omnivore in the second level to species in
high trophic levels. For most species Hgr was positively correlated with size, and this
increase in total mercury was brought about by an increase in methyl mercury thus
validating the earlier model. Hgr also increased with trophic level.
More recently, Lawson and Mason (1998) demonstrated that different ligands influenced the uptake of inorganic mercury/methyl mercury by phytoplankton
(Thalassiosira weissflogii) which are at the base of the estuarine food chain. Copepods and amphipods feeding on the algal cells assimilated methyl mercury more efficiently than inorganic mercury. Finally, fish feeding on the copepods assimilated methyl mercury more efficiently than inorganic mercury because of the larger fraction
of methyl mercury found in the tissues of the copepods.
13.6.2
Human Exposure to Methyl Mercury
The major source of mercury in the human diet is from the consumption of fish. Most
edible fish contain low amounts of methyl mercury in their tissues (up to 200 ng g-l)
(WHO/PCS 1990). Predatory species (ocean tuna, shark, swordfish and fresh-water species such as pike and walleye) may contain methyl mercury in excess of! 000 ng g-l.
Mediterranean tuna are known to reach 4500 ng g-l (Bernhard 1985). Poisonings in
Japan by the consumption of fish containing methyl mercury demonstrated the neurological damage and teratogenic effects of mercury on human populations. Damage
is now known to be mainly psychomotor disturbances and mental retardation
(Skerfving 1991). Chromosome damage has also been reported (Skerfving 1970).
13.6
Mercury in the Marine Food Chain
13.6.1
Bioaccumulation
255
The production of methyl mercury in aquatic systems is the first stage in the aquatic
bioaccumulation process (WHO/IPCS 1990). Bioaccumulation is distinct from
biomagnification (Mance 1987). Bioaccumulation involves the uptake from water independently by each trophic level and species, whereas biomagnification involves the
transfer from one trophic level to another by ingestion. Forstner and Wittmann (1979)
concluded that because of its high affinity for organic substances, mercury (together
with arsenic) was likely to show biomagnification of the food chain. There is, however, conflicting evidence in the literature. Some studies have reported an increase along
the food chain (e.g. Knauer and Martin 1972), whereas others have shown no consistent increase (e.g. Leatherland and Burton 1975). It has been shown, however, that Hgr
concentrations and the percentage of methyl mercury increase in older organisms and
those at the top of the food chain (Bernhard 1985, 1988). It was suggested, from models, that this is brought about because the inorganic mercury reaches a constant concentration early in the lifespan, while that for methyl mercury increases with the size
of the specimen and the trophic level of the species.
Minganti et al. (1996) studied the accumulation of mercury along the web of seafood species in the Ligurian Sea. They investigated five crustaceans, whose trophic
positions in the food web from herbivore/omnivore in the second level to species in
high trophic levels. For most species Hgr was positively correlated with size, and this
increase in total mercury was brought about by an increase in methyl mercury thus
validating the earlier model. Hgr also increased with trophic level.
More recently, Lawson and Mason (1998) demonstrated that different ligands influenced the uptake of inorganic mercury/methyl mercury by phytoplankton
(Thalassiosira weissflogii) which are at the base of the estuarine food chain. Copepods and amphipods feeding on the algal cells assimilated methyl mercury more efficiently than inorganic mercury. Finally, fish feeding on the copepods assimilated methyl mercury more efficiently than inorganic mercury because of the larger fraction
of methyl mercury found in the tissues of the copepods.
13.6.2
Human Exposure to Methyl Mercury
The major source of mercury in the human diet is from the consumption of fish. Most
edible fish contain low amounts of methyl mercury in their tissues (up to 200 ng g-l)
(WHO/PCS 1990). Predatory species (ocean tuna, shark, swordfish and fresh-water species such as pike and walleye) may contain methyl mercury in excess of! 000 ng g-l.
Mediterranean tuna are known to reach 4500 ng g-l (Bernhard 1985). Poisonings in
Japan by the consumption of fish containing methyl mercury demonstrated the neurological damage and teratogenic effects of mercury on human populations. Damage
is now known to be mainly psychomotor disturbances and mental retardation
(Skerfving 1991). Chromosome damage has also been reported (Skerfving 1970).