Home Research Feeds Ambient Ultrafine Particle Ingestion Alters Gut Microbiota in Association with Increased Atherogenic Lipid Metabolites

Ambient Ultrafine Particle Ingestion Alters Gut Microbiota in Association with Increased Atherogenic Lipid MetabolitesOriginal paper

Researched by:

  • Karen Pendergrass

Last Updated: 2026-07-04

Karen Pendergrass
Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.

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Location
United States of America
Sample Site
Caecum
Species
Mus musculus

What was studied?

Researchers tested whether orally ingested ambient ultrafine particles (UFP, under 0.1 to 0.2 micrometers) alter gut microbiota and promote atherogenic lipid metabolites. The model used low density lipoprotein receptor null (Ldlr-null) mice on a high-fat diet, a standard atherosclerosis model.

How was it studied?

Male Ldlr-null mice received oral gavage of 40 micrograms of collected freeway UFP or vehicle control, 3 days a week for 10 weeks (n=11 to 12 per group). Cecal microbiota was profiled by 16S rRNA MiSeq sequencing, and intestinal and plasma lipid metabolites were quantified by mass spectrometry.

What did they find?

UFP ingestion increased Verrucomicrobia abundance by about 133 percent while decreasing Firmicutes by 19 percent, Cyanobacteria by 98 percent, and Actinobacteria by 40 percent, with reduced overall diversity. Intestinal lysophosphatidylcholine (LPC 18:1) rose 1.8-fold and plasma LPC 18:1 rose about 6.5-fold; cecal cholesterol increased 1.25-fold while coprostanol fell 69 percent. Actinobacteria, Cyanobacteria, and Firmicutes were inversely correlated with plasma LPC 18:1 levels.

Why it matters

The findings link inhaled air pollution particles, ingested via mucociliary clearance into the gut, to dysbiosis and pro-atherogenic lipid changes. This supports a gut-vascular axis by which ambient particulate exposure could contribute to atherosclerosis risk.

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