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reported the following residues of 2,3,7,8-TCDD. Further details of this study are given
in Norstrom et al. 1986.
Lake Ontario, early 1970s
2-5 μg/kg (i.e., 0.002-0.005 ppm by weight)
Lake Ontario, 1984/1985
0.08-0.1 μg/kg
Lake Michigan, 1971
0.25 μg/kg
Lake Michigan, 1972
0.07 μg/kg
Lake Michigan, 1984/1985
0.001-0.002 μg/kg
In another study conducted during 1983-85, fish from the Baltic Sea were found to
contain 0.003-0.029 μg/kg of 2,3,7,8-TCDD (Rappe et al. 1987).
Recognizing the widespread occurrence of PHAHs in the natural environment,
interest has grown in the development of simple rapid assays that can be used in a
cost-effective way to identify “hot spots,” where there are particularly high levels
of them. Indeed, a wide range of tests are now available that are suitable for such
biomonitoring (Persoone et al. 2000). In the next section, details will be given of the
CALUX assay, which is based on a line of rat hepatoma cells that are responsive to
“dioxin-like” compounds. This assay has been used for environmental monitoring. In
one study, sediments were sampled from coastal and inland sites in the Netherlands
and assayed for dioxin-like activity (Stronkhurst et al. 2002). The importance of this
approach is that it measures the operation of a toxic mechanism in environmental
samples and so brings to attention particular areas that require further investigation.
Once hot spots have been identified, chemical analysis and biomarker assays can be
used, which are expensive and time-consuming, to gain more detailed information
about the nature and scale of the problem.
7. 5 to x I c I t y
2,3,7,8-TCDD is a compound of very high toxicity to certain mammals, and there
has been great interest in the elucidation of its mode of action. The situation is com-
plicated, at least on the surface, by the variety of symptoms associated with dioxin
toxicity. Symptoms include dermal toxicity, immunotoxicity, reproductive effects,
teratogenicity, and endocrine toxicity, which, together with induction of CYP1A,
have been associated with the very strong binding of this molecule to the Ah recep-
tor. These toxic effects have been referred to collectively as
Ah-receptor-mediated
toxicity
. Interestingly, a strain of mice deficient in the Ah receptor do not respond
in this way to 2,3,7,8-TCDD or to related compounds that behave in a similar way
(Fernandez-Salguero et al. 1996). Although this observation supports the idea that
toxicity is being mediated through the Ah receptor, it does not prove that this is the
case. Until the mechanisms are known by which this toxicity is expressed, there will
remain questions about whether this toxicity is truly mediated through this receptor,
or whether this occurs through another receptor (or receptors) with similar binding
properties to the Ah receptor, which is similarly affected by dioxin-like compounds.
There is a further potential problem; it is well known that cytochrome P450 1A1 has
a marked capacity to activate planar compounds such as PAHs or coplanar PCBs.
To what extent, then, is Ah-receptor-mediated toxicity simply a consequence of the
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