Environmental occurrence, abundance, and potential toxicity of polychlorinated biphenyl congeners: considerations for a congener-specific analysis.

Abstract

Polychlorinated biphenyls (PCBs) as environmental contaminants often cannot be adequately described by reference to Aroclors or to total PCBs. Although there are 209 possible PCB configurations (congeners), perhaps half that number account for nearly all of the environmental contamination attributable to PCBs. Still fewer congeners are both prevalent and either demonstrably or potentially toxic. If potential toxicity, environmental prevalence, and relative abundance in animal tissues are used as criteria, the number of environmentally threatening PCB congeners reduces to about thirty-six. Twenty-five of these account for 50 to 75% of total PCBs in tissue samples of fish, invertebrates, birds, and mammals.A few PCB congeners that are sterically similar to 2,3,7,3,7, are directly toxic. Other PCB congeners, as well as those that are directly toxic, may also be involved in toxicity indirectly by stimulating the production of (inducing) bioactivating enzyme systems. The most consequential of these have the ability to induce aryl hydrocarbon metabolizing mixed-function oxidases (MFOs). A result can be an increased capacity for bioactivation of otherwise nontoxic foreign compounds such as certain polynuclear aromatic hydrocarbons (PAH) to cytotoxic or genotoxic metabolites. The effectiveness of specific PCB congeners as inducers of different types of cytochrome P-450-dependent MFO systems is determined by their stereochemistry. Although MFO induction is not a proximate cause, it is a strong correlate of certain kinds of toxicities. Structural patterns can thus be used to discriminate among PCB congeners on the basis of toxic potential, if not entirely on toxicity per se. Congeners that demonstrate 3-methylcholanthrene-type (3-MCtype) and mixed-type MFO induction have the greatest toxic potential. These congeners most closely resemble 2,3,7,8-TCDD in their structures and in their toxic effects. The larger group of phenobarbital-type (PBtype) inducers have considerably less potential for contributing to toxic effects. Weak inducers and noninducing congeners have the least potential for toxicity.Using the rationale described in this paper, we assigned the most environmentally threatening PCB congeners to four groups. Congeners assigned to Group 1 are considered most likely to contribute to adverse biological effects attributable to PCBs in an environmental sample. Group 1A contains the three most potent (pure 3-MC-type inducer) congeners, IUPAC numbers 77, 126, and 169. Six congeners, numbers 105, 118, 128, 138, 156, and 170, are assigned to Group 1B. These congeners are mixed-type inducers that have been reported frequently in environmental samples. Group 2 congeners are PB-type inducers that are also prevalent in the environment; these include numbers 87, 99, 101, 153, 180, 183, and 194. Group 3 congeners, numbers 18,44,49,52,70,74, 151, 177, 187, and 201, are weak or noninducers, but they occur frequently in the environment or in high concentrations in animal tissues relative to other PCB congeners, and so may be of ...

Accumulation of Polychlorinated Biphenyls (PCBs) and Evaluation of Hematological and Immunological Effects of PCB Exposure on Turtles

“…Exposure to PCBs in red-eared slider turtles is characterized by low concentrations of moderately chlorinated mono-ortho and di-ortho congeners (penta-, hexa-, and hepta-CBs). Congeners with 5-7 chlorine atoms are prevalent in the environment because they occur in greater proportions in many PCB formulations (McFarland and Clarke 1989). They are more often found in biota because they are not readily metabolized compared to less chlorinated PCBs, but also do not tightly bind to soil and sediment as do congeners with high chlorination (McFarland and Clarke 1989).…”

“…Congeners with 5-7 chlorine atoms are prevalent in the environment because they occur in greater proportions in many PCB formulations (McFarland and Clarke 1989). They are more often found in biota because they are not readily metabolized compared to less chlorinated PCBs, but also do not tightly bind to soil and sediment as do congeners with high chlorination (McFarland and Clarke 1989). Polychlorinated biphenyl 153 (di-ortho) has been reported as the dominant PCB congener in many studies because it is not as easily biotransformed as other congeners (Safe 1984).…”

Regulation of estrogen receptor beta activity and implications in health and disease

“…Polychlorinated biphenyls (PCBs) are environmental contaminants that have been found at high levels in human samples, like adipose tissue, breast milk, and ovarian follicle fluid [71][72][73]. Depending on their chemical structure, PCBs may act disruptive on estrogen, androgen, or thyroid hormone receptors and have been demonstrated to exert numerous adverse effects on reproduction, the immune system, and development [74][75][76][77].…”

Chirality as an Environmental Forensics Tool

“…Field studies have inferred POP biotransformation from lower measured biotransformation factors (i.e. lower relative concentrations in predator body residues compared to that in prey), lower concentrations relative to recalcitrant congeners such as PCB 153, or lower retention of congeners expected to be metabolized based on structure-activity relations [206][207][208][209][210][211]. However, these methods are indirect and do not provide conclusive evidence for in vivo biotransformation, underscoring the difficulty in unequivocally detecting biotransformation in aquatic food webs using achiral techniques alone, without the use of stable-carbon or radiolabeled tracers and the expenses involved therein.…”

“…Both PCBs 95 and 136 have vicinal meta/para hydrogen atoms, making them amenable to attack by CYP2B isozymes. It is not clear if CYP2B-like isozymes can be induced in fish [228,229], but if this degradation was catalyzed by CYP2B, then it is clear that conventional models of predicting CYP-mediated PCB degradation [206][207][208][209][210][211] do not properly account for enantiomer-specific degradation. Wiberg et al [230] suggested that the difference in degradation of these two congeners could be attributed to changes in chemical assimilation across the gastrointestinal tract from hydrophobicity and steric hindrance.…”