Unless it can be shown otherwise we must assume that dioxins, furans, PCBs and others will add together to give a total dioxin-like toxicity.
This has been shown experimentally for dioxins and furans (Eadon, 1986), but doubts have been expressed about the validity of adding the PCBs' contribution in the same way (Goldstein & Safe, 1989). Studies have been carried out that show PCBs acting against and reducing TCDD effects.
However, a moderately toxic PCB, which produced only mild pre-birth effects in mice on its own, was found to increase TCDD effects in those mice tenfold (Birnbaum et al., 1985).
In addition:
PCBs are a mixture of dioxin-like and non-dioxin-like molecules. Some bind strongly to the Ah receptor and others only weakly.
PCBs have been reported to exert other effects separately from their action through the Ah receptor: for example there are effects on nerve signal transmission linked to a PCB which binds only weakly to the Ah receptor (Seegal et al., 1990).
Certain PCBs can increase the levels of the Ah receptor in the liver, and hence increase susceptibility to low doses of other dioxin-like compounds(Goldstein & Safe, 1989).However, laboratory investigations of interactions such as these cannot possibly cover all that are possible in humans and animals exposed in the environment to the whole range of dioxin-like compounds.
Considering both the evidence for enhancement and lessening of effects, we have to assume that the different compounds add together to produce a total dioxin-like toxicity, which can be estimated by using the TEFs given earlier.In other words, dioxins plus PCBs equals more dioxins.
ORIGINAL SOURCE
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