ArticleEnvironmental research2022
Arachidonic acid metabolism and inflammatory biomarkers associated with exposure to polycyclic aromatic hydrocarbons.
Article in Environmental research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- Air Pollution Triggers Metabolomic Signature of Mitochondrial Dysfunction in Mice and Humans: Implications for Cardiovascular Disease Development.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Nitrated Fatty Acids and Susceptibility of COPD to Air Pollution: Evidence from a Randomized Crossover Study.Environment & health (Washington, D.C.) · 2025Article
- Diesel exhaust induces gut microbiome dysbiosis and reduced fecal acetate: Role of acetate supplementation.Ecotoxicology and environmental safety · 2025Article
- Gestational exposure to particulate matter from urban wildfires is associated with changes in circulating oxylipins but not flame retardants 7 to 13 months post-exposure.Environment international · 2025Article
- Development of a metabolomic risk score for exposure to traffic-related air pollution: A multi-cohort study.Environmental research · 2024Article
- Arachidonic Acid Metabolites in Self-collected Biospecimens Following Campfire Exposure: Exploring Non-invasive Biomarkers of Wildfire Health Effects.Environmental science & technology letters · 2024Article
- Associations between Urinary Concentrations of Polycyclic Aromatic Hydrocarbons and Overactive Bladder in US Adults: Data from the National Health and Nutrition Examination Survey 2005-2016.Urologia internationalis · 2024Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Exposure to polycyclic aromatic hydrocarbons (PAHs) has been associated with systemic inflammation, yet what mechanisms regulate PAHs' inflammatory effects are less understood. This study evaluated the change of arachidonic acid (ARA) metabolites and inflammatory biomarkers in response to increased exposure to PAHs among 26 non-smoking healthy travelers from Los Angeles to Beijing. Traveling from Los Angeles to Beijing significantly increased urinary metabolites of dibenzofuran (800%), fluorene (568%), phenanthrene (277%), and pyrene (176%), accompanied with increased C-reactive protein, fibrinogen, IL-8, and IL-10, and decreased MCP-1, sCD40L, and sCD62P levels in the blood. Meanwhile, the travel increased the levels of ARA lipoxygenase metabolites that were positively associated with a panel of pro-inflammatory biomarkers. Concentrations of cytochrome P450 metabolite were also increased in Beijing and were negatively associated with sCD62P levels. In contrast, concentrations of ARA cyclooxygenase metabolites were decreased in Beijing and were negatively associated with anti-inflammatory IL-10 levels. Changes in both inflammatory biomarkers and ARA metabolites were reversed 4-7 weeks after participants returned to Los Angeles and were associated with urinary PAH metabolites, but not with other exposures such as secondhand smoke, stress, or diet. These results suggested possible roles of ARA metabolic alteration in PAHs-associated inflammatory effects.
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