Environmental research · 2026
Short-term exposure to ambient air pollution, gut microbiota, and pro-atherosclerotic responses in healthy adults: A prospective panel study.
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He Xinghou, Zhao Erlu, Song Xiaoming, Zhao Qian, Liu Jiahui, Zhang Bin, Xu Huiying, Fang Yan, Wei Xiangrui, Zhu Yutong, Xu Hongbing, Wang Tong, Huang Wei
Аннотация
BACKGROUND: Evidence shows that air pollution exposure is associated with an increased risk of cardiovascular diseases, and gut microbiota may serve as biological intermediates. However, the underlying mechanisms and possible metabolic pathways remain unclear.
METHODS: A prospective panel study was conducted among 152 healthy young adults in Beijing, China, who were engaged in four rounds of follow-ups from September 21, 2019, to January 5, 2020. Gut microbiota, fecal metabolites, and serum biomarkers of pro-inflammatory (e.g., citrullinated histone-H3, interleukin-1β, neutrophil elastase, myeloperoxidase, and monocyte chemotactic protein-1) and pro-atherosclerotic responses (e.g., soluble intercellular adhesion molecule-1, vascular endothelial growth factor-A, lipoprotein-associated phospholipase-A2, matrix metalloproteinase-8, and P-selectin) were measured during follow-ups. Linear mixed-effects models were used to estimate the associations between air pollutants and health data. Mediation and functional analyses were performed to evaluate whether gut microbiota mediated the alterations in pro-inflammatory and pro-atherosclerotic biomarkers, and to identify potential metabolic pathways.
RESULTS: Interquartile range increases in ambient air pollutants, including fine particulate matter, black carbon, nitrogen dioxide, ozone, sulfur dioxide, and carbon monoxide at prior up to 24 hours were associated with 1.4% (95% CI: 0.05-2.8) to 248.0% (95% CI: 82.6-413.3) increases in biomarkers of pro-inflammatory and pro-atherosclerotic responses. Significant decreases in alphadiversity (as measured by Shannon, Simpson, and Chao1) and alterations in the composition of gut microbiota were also observed in association with air pollution exposure. Specifically, the abundance of several microbial species such as Anaerostipes hadrus, Laedolimicola ammoniilytica, and Ruminococcus callidus may act as potential mediators, accounting for an estimated 7.9% to 46.3% of the pro-inflammatory and pro-atherosclerotic effects of air pollution. Pathway enrichment analyses indicated that flavonoid biosynthesis, beta-alanine metabolism, and xenobiotic metabolism by cytochrome P450 may be potentially involved in these mediating effects.
CONCLUSIONS: This study provides observational evidence that gut microbiota may act as potential mediators in the detrimental subclinical cardiovascular effects of short-term air pollution exposure by modulating flavonoid biosynthesis, beta-alanine metabolism, and xenobiotic metabolism.
METHODS: A prospective panel study was conducted among 152 healthy young adults in Beijing, China, who were engaged in four rounds of follow-ups from September 21, 2019, to January 5, 2020. Gut microbiota, fecal metabolites, and serum biomarkers of pro-inflammatory (e.g., citrullinated histone-H3, interleukin-1β, neutrophil elastase, myeloperoxidase, and monocyte chemotactic protein-1) and pro-atherosclerotic responses (e.g., soluble intercellular adhesion molecule-1, vascular endothelial growth factor-A, lipoprotein-associated phospholipase-A2, matrix metalloproteinase-8, and P-selectin) were measured during follow-ups. Linear mixed-effects models were used to estimate the associations between air pollutants and health data. Mediation and functional analyses were performed to evaluate whether gut microbiota mediated the alterations in pro-inflammatory and pro-atherosclerotic biomarkers, and to identify potential metabolic pathways.
RESULTS: Interquartile range increases in ambient air pollutants, including fine particulate matter, black carbon, nitrogen dioxide, ozone, sulfur dioxide, and carbon monoxide at prior up to 24 hours were associated with 1.4% (95% CI: 0.05-2.8) to 248.0% (95% CI: 82.6-413.3) increases in biomarkers of pro-inflammatory and pro-atherosclerotic responses. Significant decreases in alphadiversity (as measured by Shannon, Simpson, and Chao1) and alterations in the composition of gut microbiota were also observed in association with air pollution exposure. Specifically, the abundance of several microbial species such as Anaerostipes hadrus, Laedolimicola ammoniilytica, and Ruminococcus callidus may act as potential mediators, accounting for an estimated 7.9% to 46.3% of the pro-inflammatory and pro-atherosclerotic effects of air pollution. Pathway enrichment analyses indicated that flavonoid biosynthesis, beta-alanine metabolism, and xenobiotic metabolism by cytochrome P450 may be potentially involved in these mediating effects.
CONCLUSIONS: This study provides observational evidence that gut microbiota may act as potential mediators in the detrimental subclinical cardiovascular effects of short-term air pollution exposure by modulating flavonoid biosynthesis, beta-alanine metabolism, and xenobiotic metabolism.