Development of a neurotoxic equivalence scheme of relative potency for assessing the risk of PCB mixtures

Atmospheric polychlorinated biphenyls in Indian cities: Levels, emission sources and toxicity equivalents

“…Neurotoxic Equivalency Factors (NEFs) were evaluated for the observed PCB congeners as developed by Simon et al (2007) in the same fashion that the dioxin TEQ scheme represents the Ah-receptor related toxicity.…”

“…Corresponding to 12 dl-PCBs, the remaining congeners are referred to as the non-dioxin-like congeners (ndl-PCB). Although these congeners exert weak or no effect on Ah-receptors but they interfere with intracellular signaling pathways that are regulated and modulated by Ca 2þ , such as those involving ryanodine receptors, protein kinase C, inositol triphosphate or arachidonic acid, and, thus, cause neurotoxicity (Kodavanti, 2004;Simon et al, 2007).…”

“…Corresponding to 12 dioxin-like PCB congeners, the remaining congeners are referred to as the nondioxin-like congeners (ndl-PCB). These congeners exert weak or no effect on Ah-receptors; however, they interfere with intracellular signaling pathways that are regulated and modulated by Ca 2þ , such as those involving ryanodine receptors, protein kinase C, inositol triphosphate or arachidonic acid, and, thus, cause neurotoxicity (Simon et al, 2007). This paper reports (i) occurrence of PCBs in the atmosphere of seven major Indian cities, (ii) evaluates potential source regions of measured PCBs using two different Lagrangian transport models (HYSPLIT and FLEXPART), (iii) estimates toxicity equivalents associated with inhalation exposure to PCBs.…”

Uptake of radiolabeled 3,3′,4,4′‐tetrachlorobiphenyl into Japanese quail egg compartments and embryo following air cell and albumen injection

“…Species-specific exposure to PCBs is influenced by many factors, such as movement and availability of the contaminant, biomagnification, absorption, and metabolism. They cause a range of effects in vertebrates including developmental deformities, cancers, neurodevelopmental changes, immune effects, and endocrine disruption [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15].…”

“…These congeners activate the aryl hydrocarbon receptor, which causes a series of downstream effects on cytochrome P450s that can result in toxicity [16][17][18][19][20][21][22]. The effects of the non-dioxin-like congeners are less clear, but they have been implicated in many of the carcinogenic, neurotoxic, and endocrine-disrupting effects [6,14,16]. Postulated mechanisms of action include binding the ryanodine receptor [23], nitric oxide synthase effects [24], apoptosis [25], alterations to membrane structure [26], dopamine depletion [27,28], reactive oxygen species formation [29], and effects on neural protein kinase C [14].…”