been debarred in many nations since 1970, yet these contaminants represent a
significant class of priority contaminants due to their long bioaccumulation, persistence and toxicity (Leoni and Biocca 1978; Birnbaum and Staskal-Wikoff 2010;
Chatel et al. 2017; Adams et al. 2019). Of 209 congeners of PCBs, 78 show axial
chirality in their non-planar conformation, 19 of which form stable enantiomers
(atropisomers) owing to restricted rotation around the central carbon atom (see
Chap. 2). Because of these facts, the toxicity of PCBs on terrestrial and marine
biota has been a priority research focus of the past decades (Ahlborg and Hanberg
1994; Hamm et al. 2003; Spano et al. 2005; La Rocca and Mantovani 2006; Jofre
and Karasov 2008; National Toxicology Program 2010; Slater et al. 2011; Jepson
et al. 2016; Lang et al. 2018; Petriello et al. 2018; Kaya et al. 2019; Schnitzler et al.
2019). It has been reported that the non-ortho coplanar PCBs show the highest
toxicity trailed by the moderately toxic mono ortho coplanar congeners, whereas the
di-ortho substituted PCBs turned out to show a low toxicity (Kannan et al. 1988;
Hansen and Robertson 2008). The unlike toxicity of these PCBs comprises porphyria, weight loss, teratogenesis, productive malfunctions and endocrine disturbances in various organisms (Kubota et al. 2004; Hansen and Robertson 2008).
Ahlborg and Hanberg (1994) offered a toxic equivalency model by which authors
reported the toxicity of PCB congeners. The authors evaluated the toxic equivalency
factors (TEFs) for PCBs. Each PCB had been allocated a TEF value based on its
toxicity relative to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) that has by definition a TEF of 1.00. This TEF system is based on the same principles as earlier
described for polychlorinated dibenzo-p-dioxins and furans (PCDD/F); for details,
see Safe (1990) and Stahl et al. (1992).
The toxicity of chiral, atropisomeric PCBs and their methylsulfone and hydroxylated transformation products has been subject for recent studies. Several examples
are listed below.
Recently, Li et al. reported on the toxicokinetics of PCB 136 enantiomers in mice
experiments (Li et al. 2019). The authors studied the enantioselective toxicokinetics
a Cyp P450 metabolism. The toxicokinetic analysis of the experiments revealed
gender and genotype-dependent differences in toxicokinetic parameters for the here
investigated PCB 136 atropisomers and its metabolites.
By applying the Zebrafish model (Danio rerio) under laboratory conditions, Chai
et al. (2018) identified atropisomer-selective effects for PCB 91 enantiomers.
Enantiomer-selective effects expressed in tubular necrosis and cellular hypertrophy
in the fish kidney development were identified. The author concluded that the high
mortality after rac-/(+)-PCB91 exposure may be caused by neurotoxic effects, while
the high mortality after (–)-PCB91 exposure may be caused by on kidney failure.
An updated summary on the toxicological effects of atropisomeric PCBs is
reported in a recent review (Kania-Korwel and Lehmler 2016a, b) with reference
to all 19 chiral PCBs. Here, both toxicokinetics and relevant effect and elimination
mechanisms are described and outlined. An updated list of selected references on the
enantioselective toxicity of PCBs and their transformation products is provided here
for further readings (Lehmler et al. 2005; Pessah et al. 2009, Kania-Korwel et al.
10.2 Toxicity of Chiral Pollutants
281
significant class of priority contaminants due to their long bioaccumulation, persistence and toxicity (Leoni and Biocca 1978; Birnbaum and Staskal-Wikoff 2010;
Chatel et al. 2017; Adams et al. 2019). Of 209 congeners of PCBs, 78 show axial
chirality in their non-planar conformation, 19 of which form stable enantiomers
(atropisomers) owing to restricted rotation around the central carbon atom (see
Chap. 2). Because of these facts, the toxicity of PCBs on terrestrial and marine
biota has been a priority research focus of the past decades (Ahlborg and Hanberg
1994; Hamm et al. 2003; Spano et al. 2005; La Rocca and Mantovani 2006; Jofre
and Karasov 2008; National Toxicology Program 2010; Slater et al. 2011; Jepson
et al. 2016; Lang et al. 2018; Petriello et al. 2018; Kaya et al. 2019; Schnitzler et al.
2019). It has been reported that the non-ortho coplanar PCBs show the highest
toxicity trailed by the moderately toxic mono ortho coplanar congeners, whereas the
di-ortho substituted PCBs turned out to show a low toxicity (Kannan et al. 1988;
Hansen and Robertson 2008). The unlike toxicity of these PCBs comprises porphyria, weight loss, teratogenesis, productive malfunctions and endocrine disturbances in various organisms (Kubota et al. 2004; Hansen and Robertson 2008).
Ahlborg and Hanberg (1994) offered a toxic equivalency model by which authors
reported the toxicity of PCB congeners. The authors evaluated the toxic equivalency
factors (TEFs) for PCBs. Each PCB had been allocated a TEF value based on its
toxicity relative to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) that has by definition a TEF of 1.00. This TEF system is based on the same principles as earlier
described for polychlorinated dibenzo-p-dioxins and furans (PCDD/F); for details,
see Safe (1990) and Stahl et al. (1992).
The toxicity of chiral, atropisomeric PCBs and their methylsulfone and hydroxylated transformation products has been subject for recent studies. Several examples
are listed below.
Recently, Li et al. reported on the toxicokinetics of PCB 136 enantiomers in mice
experiments (Li et al. 2019). The authors studied the enantioselective toxicokinetics
a Cyp P450 metabolism. The toxicokinetic analysis of the experiments revealed
gender and genotype-dependent differences in toxicokinetic parameters for the here
investigated PCB 136 atropisomers and its metabolites.
By applying the Zebrafish model (Danio rerio) under laboratory conditions, Chai
et al. (2018) identified atropisomer-selective effects for PCB 91 enantiomers.
Enantiomer-selective effects expressed in tubular necrosis and cellular hypertrophy
in the fish kidney development were identified. The author concluded that the high
mortality after rac-/(+)-PCB91 exposure may be caused by neurotoxic effects, while
the high mortality after (–)-PCB91 exposure may be caused by on kidney failure.
An updated summary on the toxicological effects of atropisomeric PCBs is
reported in a recent review (Kania-Korwel and Lehmler 2016a, b) with reference
to all 19 chiral PCBs. Here, both toxicokinetics and relevant effect and elimination
mechanisms are described and outlined. An updated list of selected references on the
enantioselective toxicity of PCBs and their transformation products is provided here
for further readings (Lehmler et al. 2005; Pessah et al. 2009, Kania-Korwel et al.
10.2 Toxicity of Chiral Pollutants
281