Language

English

Publication Date

7-26-2026

Journal

Viruses

DOI

10.3390/v18080823

PMID

42655643

PMCID

PMC13517826

PubMedCentral® Posted Date

7-26-2026

PubMedCentral® Full Text Version

Post-print

Abstract

Since emerging in late 2019, SARS-CoV-2 has caused over 7 million deaths globally and remains a public health concern. Understanding SARS-CoV-2 pathogenesis is vital, especially as factors like environmental exposures are still poorly understood. Polycyclic aromatic hydrocarbons (PAHs), like benzo[a]pyrene (BP), found in pollutants like cigarette smoke, diesel exhaust, and charcoal-broiled steaks, are known to injure the lungs. We aimed to evaluate if BP exacerbates SARS-CoV-2 pathogenesis in a mouse model of disease. One day following intranasal administration of BP (20 mg/kg) or vehicle control, we infected male and female K18-hACE2 mice with ancestral SARS-CoV-2 and assessed lung viral load, weight change, clinical scores, immune cell recruitment, and survival in the presence and absence of BP exposure. We found that BP-exposed mice had decreased survival compared to mock-exposed mice. Additionally, BP did not alter innate or adaptive immune cell populations in the lungs of SARS-CoV-2-infected mice. These findings suggest that PAH exposure exacerbates severe COVID-19 outcomes by unknown mechanisms, highlighting the need to further explore environmental impacts on SARS-CoV-2 infection.

Keywords

Animals, Mice, Disease Models, Animal, Male, Female, SARS-CoV-2, Benzo(a)pyrene, COVID-19, Lung, Viral Load, Polycyclic Aromatic Hydrocarbons, Humans, SARS-CoV-2, pollutant, environmental exposure, murine models

Published Open-Access

yes

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