Page 57 - The Toxicology of Fishes

Bioavailability of Chemical Contaminants in Aquatic Systems 37

The issue of greatest importance in predicting the environmental fate and effects of mercury is the
net rate of methylation (Gilmour and Henry, 1991; Ullrich et al., 2001; Winfrey and Rudd, 1990). Most
of the methylation in freshwater systems occurs in sediments, although methylation in the water column
has also been described. Anaerobic sulfur-reducing bacteria represent the primary source of MeHg in
freshwater systems (Gilmour et al., 1992) and are also active in estuarine (Compeau and Bartha, 1985)
and near-shore marine (King et al., 2001) environments. Fulvic and humic material may abiotically
methylate mercury, but the mechanism is poorly understood (Weber, 1993). Demethylation is also
mediated largely by microorganisms (Robinson and Tuovinen, 1984). Photodegradation of MeHg is
known to occur, but the end-products of this reaction and its relative contribution to the mercury cycle
are poorly understood (Sellers et al., 1996).
–
2+
In pore water that contains excess sulfide, dissolved Hg complexes with HS to form several charged
and uncharged sulfide species. Laboratory studies with sulfate-reducing bacteria suggest that the neutral
2+
0
complex HgS can diffuse across bacterial cell membranes and is the principal source of Hg for
subsequent formation of MeHg (Benoit et al., 1999, 2001). The relative concentration of each sulfide
species varies with total sulfide concentration. High sulfide concentrations favor the formation of the
–
charged species HgHS , which is thought to be poorly absorbed by microbes. The addition of sulfate
2
can stimulate methylation in sediment by providing the energy substrate for sulfate-reducing bacteria
(Gilmour et al., 1992); however, high levels of sulfate may have a negative impact on mercury methylation
due to corresponding increases in sulfide and the resultant removal of mercury from solution as HgS.
Oxides of Fe and Mn may contribute to the formation of MeHg by precipitating Hg out of the water
2+
column. The formation and dissolution of Fe and Mn oxides are controlled by the redox state and oxygen
content of water and sediment. Under the anaerobic conditions often found in sediments, these particles
2+
dissolve, making Hg available for other reactions. The presence of Fe in sediment can also reduce the
inhibitory effect of high sulfide levels on methylation rate, presumably through substrate competition
(i.e., the formation of FeS) (Furutani and Rudd, 1980; Gagnon et al., 1996).
2+
2+
Both Hg and MeHg accumulate in aquatic biota. Hg may predominate at lower trophic levels
because it comprises the largest percentage of total mercury in water and sediment. In most instances,
however, differences in dietary assimilation and retention of Hg and MeHg result in an enrichment of
2+
MeHg with each trophic level transfer. The end result is that nearly all of the mercury in fish exists as
MeHg (U.S. EPA, 1997b).
By far the largest concentration step for MeHg in the aquatic environment occurs at the base of the food
web. Reported BCFs for MeHg in freshwater primary producers (trophic level 1) average about 1 × 10 .
5
Methylmercury also biomagnifies in food webs; that is, MeHg concentrations tend to increase at succes-
sively higher trophic levels. BMFs for MeHg in freshwater forage fish (concentration at trophic level 3/
concentration trophic level 2) and large piscivorous fish (trophic level 4/trophic level 3) range from 2 to
about 10 and average around 5 (U.S. EPA, 1997b). Altogether, biomagnification may result in a 20- to
200-fold increase in MeHg concentration from trophic level 1 to trophic level 4. These observations are
important because they suggest that factors that control uptake directly from water will determine the
amount of MeHg that enters the food web, while those that control uptake from dietary sources will
influence the extent to which biomagnification occurs at higher trophic levels.
The dominant form of freely dissolved MeHg in most seawater systems is MeHgCl. Uptake of MeHg
by marine phytoplankton was found to be controlled by the concentration of aqueous MeHgCl (Mason
et al., 1996). This finding is consistent with earlier work showing that MeHgCl can diffuse readily across
artificial lipid membranes (Bienvenue et al., 1984). In freshwater systems, most of the MeHg free in
solution exists as MeHgOH. Watras et al. (1998) reported that MeHg concentrations in microseston from
15 freshwater lakes correlated with modeled concentrations of MeHg (free ion) or MeHgOH, but not
MeHgCl; however, the diffusion rate for MeHgOH across biological membranes is only 0.04 times that
of MeHgCl (Mason et al., 1996). For this reason, Watras et al. (1998) speculated that the uptake of
MeHg by microseston was controlled by an active transport mechanism. MeHg complexed with cysteine,
thiourea, or thioglycolate was taken up directly from water by sheepshead minnows (Leaner and Mason,
2001). In mammals, MeHg–cysteine complexes are actively transported across placental membranes and
the blood–brain barrier by a neutral amino acid carrier system (Kajiwara et al., 1996; Kerper et al.,
1992). It is not known whether this or a similar mechanism is active in aquatic biota.