Although the acute toxicity of benzo(a)pyrene (B[a]P) has been extensively studied, this review addresses the long-term and transgenerational toxicity of B[a]P to aquatic species and humans, integrating evidence from both in vivo and in vitro studies. The paper provide an integrated analysis of several experimental models, offering a more comprehensive understanding of the toxicity mechanisms and potential ecological impacts. Early exposure generates mutagenic DNA adducts that persist throughout life, giving rise to precancerous lesions. Carcinogenicity, teratogenicity, immunotoxicity and neurotoxicity represent the most dangerous health effects. Species-specific differences in transcriptomic responses highlight that not all species respond equally to B[a]P pollution. Some populations develop genetic resistance through a desensitized AhR signaling pathway; this adaptation carries significant and persistent transgenerational fitness costs, including altered metabolism and reduced reproductive capacity, which persist despite site remediation. Effective risk assessment requires integrating population exposure history with in vivo validation, to account for population-specific metabolic responses.

Benzo[a]pyrene toxicity: A critical review on long-term health impacts in aquatic species and humans

Santacroce, Maria Pia
Writing – Original Draft Preparation
;
Pugliese, Nicola
Writing – Review & Editing
;
Perillo, Antonella
Writing – Original Draft Preparation
;
Giudice, Adriana Lo
Formal Analysis
;
Buonfrate, Valeria
Data Curation
;
Tinelli, Antonella
Writing – Review & Editing
2026-01-01

Abstract

Although the acute toxicity of benzo(a)pyrene (B[a]P) has been extensively studied, this review addresses the long-term and transgenerational toxicity of B[a]P to aquatic species and humans, integrating evidence from both in vivo and in vitro studies. The paper provide an integrated analysis of several experimental models, offering a more comprehensive understanding of the toxicity mechanisms and potential ecological impacts. Early exposure generates mutagenic DNA adducts that persist throughout life, giving rise to precancerous lesions. Carcinogenicity, teratogenicity, immunotoxicity and neurotoxicity represent the most dangerous health effects. Species-specific differences in transcriptomic responses highlight that not all species respond equally to B[a]P pollution. Some populations develop genetic resistance through a desensitized AhR signaling pathway; this adaptation carries significant and persistent transgenerational fitness costs, including altered metabolism and reduced reproductive capacity, which persist despite site remediation. Effective risk assessment requires integrating population exposure history with in vivo validation, to account for population-specific metabolic responses.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11586/592040
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