The Carcinogenic Properties of Overlooked yet Prevalent Polycyclic Aromatic Hydrocarbons in Human Lung Epithelial Cells

The WHO classified air pollution as a human lung carcinogen and polycyclic aromatic hydrocarbons (PAHs) are components of both indoor (e.g., tobacco smoke and cookstoves) and outdoor (e.g., wildfires and industrial and vehicle emissions) air pollution, thus a human health concern. However, few studi...

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Published in:	Toxics (Basel) Vol. 10; no. 1; p. 28
Main Authors:	Bauer, Alison K, Siegrist, Katelyn J, Wolff, Melanie, Nield, Lindsey, Brüning, Thomas, Upham, Brad L, Käfferlein, Heiko U, Plöttner, Sabine
Format:	Journal Article
Language:	English
Published:	Switzerland MDPI AG 09-01-2022 MDPI
Subjects:	1-methylanthracene Adducts Air pollution Apoptosis Benzo(a)pyrene Benzo(a)pyrene-diol-epoxide Binary mixtures Cancer Carcinogens Cell cycle Cell death Cell interactions Cell lines Communication Cytochrome Cytotoxicity Deoxyribonucleic acid DNA DNA adducts Emissions Environmental health Epithelial cells Epithelium Evaluation Experiments Fluoranthene Gap junctions Indoor air quality Industrial pollution Low molecular weights Lungs Micronuclei Molecular weight Polycyclic aromatic hydrocarbons Public health Tobacco Toxicity Vehicle emissions Wildfires United States > US Germany co-carcinogenic lung gap junctions fluoranthene benzo[a]pyrene epithelial cells micronuclei polycyclic aromatic hydrocarbons 1-methylanthracene
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Summary:	The WHO classified air pollution as a human lung carcinogen and polycyclic aromatic hydrocarbons (PAHs) are components of both indoor (e.g., tobacco smoke and cookstoves) and outdoor (e.g., wildfires and industrial and vehicle emissions) air pollution, thus a human health concern. However, few studies have evaluated the adverse effects of low molecular weight (LMW) PAHs, the most abundant PAHs in the environment. We hypothesized that LMW PAHs combined with the carcinogenic PAH benzo[ ]pyrene (B[ ]P) act as co-carcinogens in human lung epithelial cell lines (BEAS-2B and A549). Therefore, in this paper, we evaluate several endpoints, such as micronuclei, gap junctional intercellular communication (GJIC) activity, cell cycle analysis, -BPDE-DNA adduct formation, and cytotoxicity after mixed exposures of LMW PAHs with B[ ]P. The individual PAH doses used for each endpoint did not elicit cytotoxicity nor cell death and were relevant to human exposures. The addition of a binary mixture of LMW PAHs (fluoranthene and 1-methylanthracene) to B[ ]P treated cells resulted in significant increases in micronuclei formation, dysregulation of GJIC, and changes in cell cycle as compared to cells treated with either B[ ]P or the binary mixture alone. In addition, -BPDE-DNA adducts were significantly increased in human lung cells treated with B[ ]P combined with the binary mixture of LMW PAHs as compared to cells treated with B[ ]P alone, further supporting the increased co-carcinogenic potential by LMW PAHs. Collectively, these novel studies using LMW PAHs provide evidence of adverse pulmonary effects that should warrant further investigation.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	2305-6304 2305-6304
DOI:	10.3390/toxics10010028