Journal
SCIENCE OF THE TOTAL ENVIRONMENT
Volume 837, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.scitotenv.2022.155764
Keywords
Human exposure; Relative potency; Neurotoxicity; Reproductive toxicity; Endocrine-disruption; AhR mediated toxicity
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The legacy of polychlorinated naphthalenes (PCNs) persists in the environment, food, and humans, resulting in adverse effects on tissues. The disposition and retention of PCNs in tissues are influenced by molecular configuration, favoring higher chlorinated PCNs. Exposure to PCNs can lead to hepatotoxicity, neurotoxicity, immune response suppression, and endocrine disruption.
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 configu-ration 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
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