Scientists have pointed to a malfunction of the heart due to polluted air.
Researchers at the University of California, Los Angeles Medical System have discovered new biomarkers in the blood of humans and mice exposed to polluted air. They are associated with disruption of mitochondria and fat metabolism, which may explain how air pollution affects the cardiovascular system. About how polluted air can damage cells and increase the risk of diseases, see the "Izvestia" article.
Pollution disrupts cell function
The researchers found two types of metabolites in the blood samples — long-chain dicarboxylic acids (DKA) and medium- and long-chain acylcarnitines (AK). Their levels increased after exposure to pollution in both mice and humans.
The work was published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB). Previously, the research group's projects had already shown a link between air pollution and cardiovascular diseases, but the mechanism of such effects remained unclear.
The new results indicate a possible role for mitochondria, cellular structures responsible for energy production, among other things. When they are damaged, fat processing is disrupted, which causes certain metabolites to accumulate in the blood.
The level of special substances in the blood has increased
To detect the changes, the scientists analyzed blood samples obtained in two previous studies involving mice and humans. The mice were exposed to diesel exhaust for two weeks. The human part of the study involved 26 healthy, non-smoking adults from Los Angeles. In the summer of 2014 and 2015, they traveled to Beijing, where they were monitored for 10 weeks.
The researchers identified individual molecules — metabolites — and compared how their concentrations changed after contact with polluted air. In both groups, the levels of long-chain DKA and AK of the medium and long chain increased.
Mitochondria stop coping
DKA and AK have previously been linked to impaired fatty acid oxidation, a process that helps cells obtain energy from fats. One of the causes of such disorders may be mitochondrial dysfunction.
According to scientists, the accumulation of these substances may indicate cellular stress and damage to lipids in the liver. Such changes are considered as one of the possible early effects of exposure to polluted air on the body.
Thus, mitochondrial disorders may be one of the mechanisms linking air pollution with subsequent cardiovascular consequences. The researchers note that the data obtained helps to better understand the changes taking place in the body even before the appearance of pronounced diseases.
Scientists compared humans and mice
An important part of the work was the comparison of the results of the two studies. Scientists were looking for changes that manifested themselves after air pollution in both animals and humans.
In an experiment with mice, exposure to diesel exhaust was used. Participants in the human study, on the other hand, were exposed to the real urban environment during their stay in Beijing. This allowed the researchers to compare metabolic changes in different pollution exposure scenarios.
In both cases, similar changes in blood levels of DKA and AK were found. According to the authors, this coincidence supports the hypothesis that air pollution is associated with impaired fatty acid metabolism and mitochondrial function.
Biomarkers can warn about the risk
Air pollution remains a global problem, but the effects of exposure do not develop equally for all people. To date, signs of someone who will face serious consequences may become noticeable after the onset of diseases.
The researchers suggest that increasing the concentration of detected metabolites in blood plasma in the future may help identify the effects of pollution at an earlier stage. We are talking about a period when cardiovascular, metabolic or gastrointestinal diseases have not yet developed.
The authors note that the discovered biomarkers can potentially become a tool for early detection of pollution-related changes. The work so far shows a link between exposure to polluted air and metabolic disorders, rather than proving that the identified changes themselves lead to the development of a specific disease.
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