Researchers identify blood markers that reveal early biological stress from pollution exposure before chronic illness develops.
RT’s Three Key Takeaways:
- Cellular Mechanism Identified: Exposure to air pollution disrupts mitochondrial function and fatty acid metabolism, shedding light on the biological pathway linking dirty air to cardiovascular disease.
- Novel Blood Biomarkers: Researchers discovered elevated circulating levels of dicarboxylate acids and acyl-carnitines in both animal models and human subjects exposed to pollution, according to findings published in Arteriosclerosis, Thrombosis, and Vascular Biology.
- Early Risk Detection: Measuring these specific blood metabolites could allow healthcare providers to identify pollution-induced tissue stress in healthy patients before irreversible cardiovascular, metabolic, or gastrointestinal damage occurs, the researchers noted.
Investigators at UCLA Health have discovered novel blood biomarkers that explain how exposure to air pollution damages cellular health and elevates the risk of cardiovascular disease, according to a study published in Arteriosclerosis, Thrombosis, and Vascular Biology.
While epidemiologic studies have long connected contaminated air with adverse cardiovascular outcomes, the precise cellular pathways triggering heart disease have remained unclear, according to the release. The new findings pinpoint the mitochondria—the energy-producing structures of cells—as a primary driver in this disease cascade, the authors stated.
Mitochondrial Dysfunction and Lipid Buildup
When ambient air pollution damages cellular mitochondria, the cells lose their ability to efficiently break down dietary and stored fats for energy, according to UCLA Health researchers. As a consequence of impaired fatty acid oxidation, intermediate breakdown products—specifically long-chain dicarboxylate acids (DCAs) and medium- to long-chain acyl-carnitines (ACs)—accumulate and circulate within the bloodstream, the researchers found.
According to the study team, the buildup of these specific metabolites reflects hepatic oxidative stress and lipid damage, an inflammatory condition that can subsequently advance to chronic cardiovascular disease.
Cross-Species Analysis
To isolate the biological indicators, the investigative team analyzed plasma samples drawn from two prior cohorts, according to the research report. In a preclinical model, mice were subjected to diesel exhaust inhalation over a two-week period. In a companion human trial, 26 healthy, nonsmoking adults from Los Angeles traveled to Beijing during the summer months of 2014 and 2015, where their clinical markers were tracked for 10 weeks, the authors reported.
By cataloging individual metabolic molecules in both sets of blood samples, researchers observed identical patterns: exposure to pollution resulted in substantial increases in circulating long-chain DCAs and medium-to-long-chain ACs across both mice and humans, according to the data. Because these metabolites are well-established indicators of fatty acid metabolic deficits, the results confirm that mitochondrial injury plays an early role in cardiovascular damage caused by poor air quality, the study authors stated.
Opportunities for Early Clinical Intervention
Although environmental air pollution poses global public health concerns, clinical manifestations vary widely, with only a portion of exposed individuals developing debilitating conditions, according to the UCLA Health release. Presently, clinicians possess few predictive tools to evaluate susceptibility until late-stage disorders emerge, including heart disease, diabetes, dyslipidemia, fatty liver disease, or cancer.
Testing for elevations in these circulating blood metabolites could allow healthcare teams to identify vulnerable patients during early stages of cellular stress, permitting clinical intervention prior to the onset of severe chronic illness, the investigators concluded.
The study was led by Jesus Araujo, MD, professor of medicine at the David Geffen School of Medicine at UCLA and professor of environmental health sciences at the UCLA Fielding School of Public Health, alongside researchers Yan Lin, Xinghua Qiu, Rajat Gupta, Gajalakshmi Ramanathan, Xinchen Lu, Fen Yin, Oliver Fiehn, Junfeng Zhang, Joel D. Kaufman, Yifang Zhu, and Michael Rosenfeld. Funding was provided by the National Institute of Environmental Health Sciences (NIEHS), the National Institutes of Health (NIH), the AHA, the National Key Research and Development Program of China, and the National Natural Science Foundation of China.
