ArticleEnvironmental toxicology and pharmacology2022
Chronic exposure to traffic-related air pollution reduces lipid mediators of linoleic acid and soluble epoxide hydrolase in serum of female rats.
Article in Environmental toxicology and pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Long-term exposure to air pollution and metabolites in children and young adults in a Swedish birth cohort.Journal of exposure science & environmental epidemiology · 2026Article
- Article
- Delayed viral clearance and altered inflammatory responses affect severity of SARS-CoV-2 infection in aged mice.Immunity & ageing : I & A · 2025Article
- Inhaled Pollutants of the Gero-Exposome and Later-Life Health.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Review
- Neuroinflammation is dependent on sex and ovarian hormone presence following acute woodsmoke exposure.Scientific reports · 2024Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic exposure to traffic-related air pollution (TRAP) is known to promote systemic inflammation, which is thought to underlie respiratory, cardiovascular, metabolic and neurological disorders. It is not known whether chronic TRAP exposure dampens inflammation resolution, the homeostatic process for stopping inflammation and repairing damaged cells. In vivo, inflammation resolution is facilitated by bioactive lipid mediators known as oxylipins, which are derived from the oxidation of polyunsaturated fatty acids. To understand the effects of chronic TRAP exposure on lipid-mediated inflammation resolution pathways, we measured total (i.e. free+bound) pro-inflammatory and pro-resolving lipid mediators in serum of female rats exposed to TRAP or filtered air (FA) for 14 months. Compared to rats exposed to FA, TRAP-exposed rats showed a significant 36-48% reduction in fatty acid alcohols, specifically, 9-hydroxyoctadecadienoic acid (9-HODE), 11,12-dihydroxyeicosatetraenoic acid (11,12-DiHETE) and 16,17-dihydroxydocosapentaenoic acid (16, 17-DiHDPA). The decrease in fatty acid diols (11,12-DiHETE and 16, 17-DiHDPA) corresponded to a significant 34-39% reduction in the diol to epoxide ratio, a marker of soluble epoxide hydrolase activity; this enzyme is typically upregulated during inflammation. The findings demonstrate that 14 months exposure to TRAP reduced pro-inflammatory 9-HODE concentration and dampened soluble epoxide hydrolase activation, suggesting adaptive immune changes in lipid mediator pathways involved in inflammation resolution.
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Registered trials
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