Trial reportParticle and fibre toxicology2023
Human exposure to diesel exhaust induces CYP1A1 expression and AhR activation without a coordinated antioxidant response.
Trial report in Particle and fibre toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Bronchial mucosal nuclear transcription factor expression and inflammatory response in humans after exposure to wood smoke.Particle and fibre toxicology · 2026Trial
- CYP1A1 as a conserved metabolic circuit linking environmental sensing to immune regulation.Archives of toxicology · 2026Review
- TET1 Protects the Lungs from Diesel Exhaust Particle-Induced Inflammation and Abnormal Function.Research square · 2026Article
- Pulmonary toxicity of brake wear particles: effects of composition and surface reactivity.Particle and fibre toxicology · 2026Article
- CYP1B1 modulates stress and repair pathways in airway cells challenged by wood smoke particles.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Article
- Causal association between circulating cytokine levels and the risk for asthma: A bidirectional, Mendelian randomization study.Medicine · 2025Article
- 4-Octyl Itaconate ameliorates diesel exhaust particle-induced oxidative stress in nasal epithelial cells.Frontiers in immunology · 2025Article
- Immunoregulation of Quercetin and Kynurenic Acid on Human Umbilical Cord Mesenchymal Stem Cells Through Gene Expression of Aryl Hydrocarbon Receptor and Interleukin-6 in Hyperglycemic Milieu.Stem cells international · 2025Article
- New insights into coordinated regulation of AHR promoter transcription; molecular mechanisms and therapeutic targets.International journal of biological sciences · 2025Review
- Acute airway inflammation following controlled biodiesel exhaust exposure in healthy subjects.Particle and fibre toxicology · 2024Article
- The single and mixed impacts of cadmium, cobalt, lead, and PAHs on systemic immunity inflammation index in male and female.Frontiers in public health · 2024Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundDiesel exhaust (DE) induces neutrophilia and lymphocytosis in experimentally exposed humans. These responses occur in parallel to nuclear migration of NF-κB and c-Jun, activation of mitogen activated protein kinases and increased production of inflammatory mediators. There remains uncertainty regarding the impact of DE on endogenous antioxidant and xenobiotic defences, mediated by nuclear factor erythroid 2-related factor 2 (Nrf2) and the aryl hydrocarbon receptor (AhR) respectively, and the extent to which cellular antioxidant adaptations protect against the adverse effects of DE.
methodsUsing immunohistochemistry we investigated the nuclear localization of Nrf2 and AhR in the epithelium of endobronchial mucosal biopsies from healthy subjects six-hours post exposure to DE (PM
resultsDE exposure caused an influx of neutrophils to the bronchial airway surface (p = 0.013), as well as increased bronchial submucosal neutrophil (p < 0.001), lymphocyte (p = 0.007) and mast cell (p = 0.002) numbers. In addition, DE exposure enhanced the nuclear translocation of the AhR and increased the CYP1A1 expression in the bronchial epithelium (p = 0.001 and p = 0.028, respectively). Nuclear translocation of AhR was also increased in the submucosal leukocytes (p < 0.001). Epithelial nuclear AhR expression was negatively associated with bronchial submucosal CD3 numbers post DE (r = -0.706, p = 0.002). In contrast, DE did not increase nuclear translocation of Nrf2 and was associated with decreased NQO1 in bronchial epithelial cells (p = 0.02), without affecting CYP1B1, aldo-keto reductases, or epoxide hydrolase protein expression.
conclusionThese in vivo human data confirm earlier cell and animal-based observations of the induction of the AhR and CYP1A1 by diesel exhaust. The induction of phase I xenobiotic response occurred in the absence of the induction of antioxidant or phase II xenobiotic defences at the investigated time point 6 h post-exposures. This suggests DE-associated compounds, such as polycyclic aromatic hydrocarbons (PAHs), may induce acute inflammation and alter detoxification enzymes without concomitant protective cellular adaptations in human airways.
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