Organometallic Compounds - Organic Pollutants: An Ecotoxicological Perspective - page 174

When TBTO is released into ambient water, a considerable proportion becomes
adsorbed to sediments, as might be expected from its lipophilicity. Studies have
shown that between 10 and 95% of TBTO added to surface waters becomes bound
to sediment. In the water column it exists in several different forms, principally the
hydroxide, the chloride, and the carbonate (Figure 8.5). Once TBT has been adsorbed,
loss is almost entirely due to slow degradation, leading to desorption of diphenyl-
tin (DPT). The distribution and state of speciation of TBT can vary considerably
between aquatic systems, depending on pH, temperature, salinity, and other factors.
TBT levels have been monitored in coastal areas of Western Europe and North
America. These have ranged upward to 5.34 μg/L in Western Europe, and 1.71 μg/L
in North America (Environmental Health Criteria 116). The highest levels were
recorded in the shallow waters of estuaries and harbors where there were large num-
bers of small boats.
TBT is taken up by aquatic organisms directly from water and from food.
Comparison of concentrations in mollusks with concentrations in ambient water
indicate very strong bioconcentration/bioaccumulation. When mollusks such as the
edible mussel ( Mytilus edulis) and the Pacific oyster ( Crassostrea gigas ) were exposed
experimentally to TBTO in ambient water, bioconcentration factors (BCFs) ranging
between 1,000-fold and 7,000-fold were found (see Environmental Health Criteria
116). With mussels exposed to relatively low levels of TBT, tissue levels were still
increasing after 7 weeks' exposure, no plateau level having been reached. Exposure
of Mytilus edulis under natural conditions indicated higher BCFs than this—5,000-
60,000-fold (Cheng and Jensen 1989). Further investigation has shown that uptake
of TBT from food can be greater than uptake directly from water. Thus, BCFs are a
reflection more of bioaccumulation than of bioconcentration in this case.
8.3.4 T of x i c i T y of f T r i b u T y l T i n
Mechanistic studies have shown that TBT and certain other forms of trialkyltin have
two distinct modes of toxic action in vertebrates. On the one hand they act as inhibitors
of oxidative phosphorylation in mitochondria (Aldridge and Street 1964). Inhibition is
associated with repression of ATP synthesis, disturbance of ion transport across the
mitochondrial membrane, and swelling of the membrane. Oxidative phosphorylation is
a vital process in animals and plants, and so trialkyltin compounds act as wide-ranging
biocides. Another mode of action involves the inhibition of forms of cytochrome P450,
which was referred to earlier in connection with metabolism. This has been demon-
strated in mammals, aquatic invertebrates and fish (Morcillo et al. 2004, Oberdorster
2002). TBTO has been shown to inhibit P450 activity in cells from various tissues of
mammals, including liver, kidney, and small intestine mucosa, both in vivo and in vitro
(Rosenberg and Drummond 1983, Environmental Health Criteria 116).
Of particular interest in the present context is that TBT can inhibit cytochrome-
P450-based aromatase activity in both vertebrates and aquatic invertebrates (Morcillo
et al. 2004, Oberdorster and McClellan-Green 2002). The conversion of testoster-
one to estradiol is catalyzed by aromatase, and so inhibition of the enzyme can, in
principle, lead to an increase in cellular levels of testosterone. The significance of
this is that many mollusks experience endocrine disruption when exposed to TBTs,