ArticleArchives of toxicology2018
Environmentally prevalent polycyclic aromatic hydrocarbons can elicit co-carcinogenic properties in an in vitro murine lung epithelial cell model.
Article in Archives of toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 60 citations in OpenAlex.
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- AhR activation triggers the synergistic genotoxicity between benzo[a]pyrene and aflatoxin B1 in metabolic-competent HepaRP cells.Archives of toxicology · 2026Article
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- Wood smoke particles elicit events associated with adverse effects in human lung epithelial cells.Frontiers in toxicology · 2026Article
- An Italian Study of PMInternational journal of molecular sciences · 2025Article
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- Polycyclic aromatic hydrocarbon exposure effects on trajectories of maternal and adolescent mental health.Child and adolescent psychiatry and mental health · 2024Article
- Premalignant Progression in the Lung: Knowledge Gaps and Novel Opportunities for Interception of Non-Small Cell Lung Cancer. An Official American Thoracic Society Research Statement.American journal of respiratory and critical care medicine · 2024Review
- Renal excretion of 1,2-dihydroxynaphthalene (DHN) in firefighting instructors after exposure to polycyclic aromatic hydrocarbons (PAHs) during live fire training.Scientific reports · 2024Article
- Modeling PAH Mixture Interactions in a Human In Vitro Organotypic Respiratory Model.International journal of molecular sciences · 2024Article
- Lung cancer associated with combustion particles and fine particulate matter (PMBiochemical pharmacology · 2023Review
- The Long Goodbye: Finally Moving on from the Relative Potency Approach to a Mixtures Approach for Polycyclic Aromatic Hydrocarbons (PAHs).International journal of environmental research and public health · 2022Article
- Article
- Strong π-stacking causes unusually large anisotropic thermal expansion and thermochromism.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Seasonal variations of polycyclic aromatic hydrocarbons in coastal sediments of a marine resource hot spot: the case of pars special economic energy zone, Iran.Environmental geochemistry and health · 2021Article
- Applicability of Scrape Loading-Dye Transfer Assay for Non-Genotoxic Carcinogen Testing.International journal of molecular sciences · 2021Review
- Cross-Sectional Estimation of Endogenous Biomarker Associations with Prenatal Phenols, Phthalates, Metals, and Polycyclic Aromatic Hydrocarbons in Single-Pollutant and Mixtures Analysis Approaches.Environmental health perspectives · 2021Article
- Two-stage 3-methylcholanthrene and butylated hydroxytoluene-induced lung carcinogenesis in mice.Methods in cell biology · 2021Article
- Airborne PAHs inhibit gap junctional intercellular communication and activate MAPKs in human bronchial epithelial cell line.Environmental toxicology and pharmacology · 2020Article
- Dietary phytochemicals as the potential protectors against carcinogenesis and their role in cancer chemoprevention.Clinical and experimental medicine · 2020Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Low molecular weight (LMW) polycyclic aromatic hydrocarbons (PAH) are the most abundant PAHs environmentally, occupationally, and are in cigarette smoke; however, little is known about their carcinogenic potential. We hypothesized that LMW PAHs act as co-carcinogens in the presence of a known carcinogen (benzo[a]pyrene (B[a]P)) in a mouse non-tumorigenic type II cell line (C10 cells). Gap junctions are commonly suppressed and inflammation induced during tumor promotion, while DNA-adduct formation is observed during the initiation stage of cancer. We used these endpoints together as markers of carcinogenicity in these lung adenocarcinoma progenitor cells. LMW PAHs (1-methylanthracene and fluoranthene, 1-10 µM total in a 1:1 ratio) were used based on previous studies as well as B[a]P (0-3 µM) as the classic carcinogen; non-cytotoxic doses were used. B[a]P-induced inhibition of gap junctional intercellular communication (GJIC) was observed at low doses and further reduced in the presence of the LMW PAH mixture (P < 0.05), supporting a role for GJIC suppression in cancer development. Benzo[a]pyrene diol-epoxide (BPDE)-DNA adduct levels were significantly induced in B[a]P-treated C10 cells and additionally increased with the LMW PAH mixture (P < 0.05). Significant increases in cyclooxygenase (Cox-2) were observed in response to the B[a]P/LMW PAH mixture combinations. DNA adduct formation coincided with the inhibition of GJIC and increase in Cox-2 mRNA expression. Significant cytochrome p4501b1 increases and connexin 43 decreases in gene expression were also observed. These studies suggest that LMW PAHs in combination with B[a]P can elicit increased carcinogenic potential. Future studies will further address the mechanisms of co-carcinogenesis driving these responses.
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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 Socratic graph.