ArticleToxicology and applied pharmacology2019
Comparative mechanisms of PAH toxicity by benzo[a]pyrene and dibenzo[def,p]chrysene in primary human bronchial epithelial cells cultured at air-liquid interface.
Article in Toxicology and applied pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 49 citations in OpenAlex.
- MicroRNA-mediated changes contributing to benzo[a]pyrene toxicity in a 3D respiratory model for asthma.Current research in toxicology · 2026Article
- Organoid for Air Pollution Toxicity Assessment: Advances and Environmental Applicability.Environment & health (Washington, D.C.) · 2025Review
- Article
- Building a predictive model for polycyclic aromatic hydrocarbon dosimetry in organotypically cultured human bronchial epithelial cells using benzo[Toxicology reports · 2025Article
- Utilization of the CometChip assay for detecting PAH-induced DNA bulky adducts in a 3D primary human bronchial epithelial cell model.Toxicology · 2025Article
- SERS and SEIRA Detection of Polycyclic Aromatic Hydrocarbons and their Derivatives in Murine Tissues: Bioaccumulation and Clearance.Journal of Raman spectroscopy : JRS · 2025Article
- Modeling PAH Mixture Interactions in a Human In Vitro Organotypic Respiratory Model.International journal of molecular sciences · 2024Article
- Innovative explorations: unveiling the potential of organoids for investigating environmental pollutant exposure.Environmental science and pollution research international · 2024Review
- Assessing susceptibility for polycyclic aromatic hydrocarbon toxicity in anFrontiers in toxicology · 2024Article
- Silicone passive sampling used to identify novel dermal chemical exposures of firefighters and assess PPE innovations.International journal of hygiene and environmental health · 2023Article
- Article
- Metabolic Activation of Benzo[International journal of molecular sciences · 2022Article
- Loading of Coal Tar in Polymeric Nanoparticles as a Potential Therapeutic Modality for Psoriasis.ACS omega · 2022Article
- Linking Coregulated Gene Modules with Polycyclic Aromatic Hydrocarbon-Related Cancer Risk in the 3D Human Bronchial Epithelium.Chemical research in toxicology · 2021Article
- Classifying polycyclic aromatic hydrocarbons by carcinogenic potency using in vitro biosignatures.Toxicology in vitro : an international journal published in association with BIBRA · 2020Article
- Airborne PAHs inhibit gap junctional intercellular communication and activate MAPKs in human bronchial epithelial cell line.Environmental toxicology and pharmacology · 2020Article
- Discovery of firefighter chemical exposures using military-style silicone dog tags.Environment international · 2020Article
- Influence of wood species on toxicity of log-wood stove combustion aerosols: a parallel animal and air-liquid interface cell exposure study on spruce and pine smoke.Particle and fibre toxicology · 2020Article
- New Approach Methods to Evaluate Health Risks of Air Pollutants: Critical Design Considerations for In Vitro Exposure Testing.International journal of environmental research and public health · 2020Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Current assumption for assessing carcinogenic risk of polycyclic aromatic hydrocarbons (PAHs) is that they function through a common mechanism of action; however, recent studies demonstrate that PAHs can act through unique mechanisms potentially contributing to cancer outcomes in a non-additive manner. Using a primary human 3D bronchial epithelial culture (HBEC) model, we assessed potential differences in mechanism of toxicity for two PAHs, benzo[a]pyrene (BAP) and dibenzo[def,p]chrysene (DBC), compared to a complex PAH mixture based on short-term biosignatures identified from transcriptional profiling. Differentiated bronchial epithelial cells were treated with BAP (100-500 μg/ml), DBC (10 μg/ml), and coal tar extract (CTE 500-1500 μg/ml, SRM1597a) for 48 h and gene expression was measured by RNA sequencing or quantitative PCR. Comparison of BAP and DBC gene signatures showed that the majority of genes (~60%) were uniquely regulated by treatment, including signaling pathways for inflammation and DNA damage by DBC and processes for cell cycle, hypoxia and oxidative stress by BAP. Specifically, BAP upregulated targets of AhR, NRF2, and KLF4, while DBC downregulated these same targets, suggesting a chemical-specific pattern in transcriptional regulation involved in antioxidant response, potentially contributing to differences in PAH potency. Other processes were regulated in common by all PAH treatments, BAP, DBC and CTE, including downregulation of genes involved in cell adhesion and reduced functional measurements of barrier integrity. This work supports prior in vivo studies and demonstrates the utility of profiling short-term biosignatures in an organotypic 3D model to identify mechanisms linked to carcinogenic risk of PAHs in humans.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.