Work

Short-term exposures to air pollutants affect mitochondrial DNA copy number in patients with acute but not in chronic coronary syndromes

Year: 2026

Type: article

Abstract: Epidemiological studies link pollution to higher coronary artery disease (CAD) risk, but the molecular pathways remain unclear. Mitochondria may play a role due to their sensitivity to pollutants. This study assesses the impact of air pollution on mitochondrial DNA copy number (mtDNAcn) in patients with angiographically documented CAD. We performed a prospective single-center cohort design by enrolling 151 patients undergoing coronary angiography in the Milan area: 89 with acute coronary syndrome (ACS), and 62 with chronic coronary syndrome (CCS). Daily levels of PM 2.5, PM 10 , and meteorological data were collected from fixed monitoring stations. Exposure was averaged over short- (1 week, 2 weeks, 3 weeks and 1 month) and long-term (1 year) periods before angiography. mtDNAcn, was measured by real-time PCR. Systemic inflammatory index (SII) was calculated from the complete blood count. ACS patients were exposed to significantly higher short-term levels of PM 2.5 and PM 10 and a greater number of days exceeding their recommended annual limits, compared to the CCS group. Multivariable linear regression showed that short-term exposure to PM 2.5 and PM 10 was inversely associated with mtDNAcn in ACS. Specifically, an interquartile range increase of 21.02 µg/m 3 in 3-week PM 2.5 , 19.13 µg/m 3 in 1-month PM 2.5 , and 23.03 µg/m 3 in 1-month PM 10 was associated with decreases in mtDNAcn of 28.00%, 29.51%, and 17.36%, respectively. mtDNAcn also negatively correlated with SII ( P = 0.028) in the study population. Short-term exposure to PM 2.5 and PM 10 is associated to reduce mtDNAcn in ACS., supporting a potential role of mitochondrial dysfunction in the pathogenesis of acute events and plaque vulnerability.

Source: Environmental Sciences Europe

DOI: 10.1186/s12302-026-01390-z