The toxicological profile of polychlorinated naphthalenes (PCNs)

The legacy of polychlorinated naphthalenes (PCNs) manufactured during the last century continues to persist in the environment, food and humans. Metrological advances have improved characterisation of these occurrences, enabling studies on the effects of exposure to focus on congener groups and indi...

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Veröffentlicht in:The Science of the total environment 2022-09, Vol.837, p.155764-155764, Article 155764
Hauptverfasser: Fernandes, Alwyn R., Kilanowicz, Anna, Stragierowicz, Joanna, Klimczak, Michał, Falandysz, Jerzy
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container_title The Science of the total environment
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creator Fernandes, Alwyn R.
Kilanowicz, Anna
Stragierowicz, Joanna
Klimczak, Michał
Falandysz, Jerzy
description The legacy of polychlorinated naphthalenes (PCNs) manufactured during the last century continues to persist in the environment, food and humans. Metrological advances have improved characterisation of these occurrences, enabling studies on the effects of exposure to focus on congener groups and individual PCNs. Liver and adipose tissue show the highest retention but significant levels of PCNs are also retained by the brain and nervous system. Molecular configuration appears to influence tissue disposition as well as retention, favouring the higher chlorinated (≥ four chlorines) PCNs while most lower chlorinated molecules readily undergo hydroxylation and excretion through the renal system. Exposure to PCNs reportedly provokes a wide spectrum of adverse effects that range from hepatotoxicity, neurotoxicity and immune response suppression along with endocrine disruption leading to reproductive disorders and embryotoxicity. A number of PCNs, particularly hexachloronaphthalene congeners, elicit AhR mediated responses that are similar to, and occur within similar potency ranges as most dioxin-like polychlorinated biphenyls (PCBs) and some chlorinated dibenzo-p-dioxins and furans (PCDD/Fs), suggesting a relationship based on molecular size and configuration between these contaminants. Most toxicological responses generally appear to be associated with higher chlorinated PCNs. The most profound effects such as serious and sometimes fatal liver disease, chloracne, and wasting syndrome resulted either from earlier episodes of occupational exposure in humans or from acute experimental dosing of animals at levels that reflected these exposures. However, since the restriction of manufacture and controls on inadvertent production (during combustion processes), the principal route of human and animal exposure is likely to be dietary intake. Therefore, further investigations should include the effects of chronic lower level intake of higher chlorinated PCN congeners that persist in the human diet and subsequently in human and animal tissues. PCNs in the diet should be evaluated cumulatively with other similarly occurring dioxin-like contaminants. [Display omitted] •PCNs elicit a range of potent toxicological effects in humans and animals•PCNs with Cl ≥5 (esp. H6CNs) have higher REPs, so are toxicologically more significant•Future studies should target chronic exposure of PCN congeners persistent in the diet
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Metrological advances have improved characterisation of these occurrences, enabling studies on the effects of exposure to focus on congener groups and individual PCNs. Liver and adipose tissue show the highest retention but significant levels of PCNs are also retained by the brain and nervous system. Molecular configuration appears to influence tissue disposition as well as retention, favouring the higher chlorinated (≥ four chlorines) PCNs while most lower chlorinated molecules readily undergo hydroxylation and excretion through the renal system. Exposure to PCNs reportedly provokes a wide spectrum of adverse effects that range from hepatotoxicity, neurotoxicity and immune response suppression along with endocrine disruption leading to reproductive disorders and embryotoxicity. A number of PCNs, particularly hexachloronaphthalene congeners, elicit AhR mediated responses that are similar to, and occur within similar potency ranges as most dioxin-like polychlorinated biphenyls (PCBs) and some chlorinated dibenzo-p-dioxins and furans (PCDD/Fs), suggesting a relationship based on molecular size and configuration between these contaminants. Most toxicological responses generally appear to be associated with higher chlorinated PCNs. The most profound effects such as serious and sometimes fatal liver disease, chloracne, and wasting syndrome resulted either from earlier episodes of occupational exposure in humans or from acute experimental dosing of animals at levels that reflected these exposures. However, since the restriction of manufacture and controls on inadvertent production (during combustion processes), the principal route of human and animal exposure is likely to be dietary intake. 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subjects adipose tissue
AhR mediated toxicity
brain
combustion
embryotoxicity
Endocrine-disruption
environment
excretion
food intake
furans
hepatotoxicity
Human exposure
human nutrition
humans
hydroxylation
immune response
liver
liver diseases
manufacturing
molecular conformation
molecular weight
Neurotoxicity
occupational exposure
polychlorinated biphenyls
Relative potency
Reproductive toxicity
title The toxicological profile of polychlorinated naphthalenes (PCNs)
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