UCLA Health identifies mitochondrial link between air pollution and heart disease

Researchers at UCLA Health have identified mitochondria as a critical link between air pollution and cardiovascular disease. By analyzing blood samples from both mice and humans, the study uncovered specific biomarkers—long-chain dicarboxylate acids (DCAs) and medium-to-long-chain acyl-carnitines (ACs)—that increase following exposure to pollutants.

The buildup of these metabolites indicates mitochondrial dysfunction, specifically an inability to properly break down fats for energy. This process suggests that air pollution triggers cellular stress, such as oxidative stress and lipid damage, which can eventually lead to heart disease. The human component of the study involved monitoring healthy, non-smoking adults from Los Angeles during travel to Beijing.

These findings complement a position paper from the European Society of Cardiology, which notes that particulate matter and gaseous pollutants like nitrogen dioxide and ozone contribute to cardiovascular mortality through systemic inflammation. According to the Global Burden of Disease study, ambient air pollution was attributable to approximately 3.1 million deaths in 2010.