THE ESSENTIAL
- Even brief exposure to high levels of ozone reduces blood oxygen saturation.
- This leads to compensatory increases in red blood cells and hemoglobin, which exacerbate arterial stiffness.
- According to the researchers, these results provide new insight into the mechanisms underlying cardiovascular damage induced by ozone exposure.
“Ozone (O3) pollution represents a significant health burden worldwide. Previous epidemiological research has linked exposure to this highly oxidizing gas to increased risk of cardiovascular diseases, including ischemic heart disease, stroke, heart failure, and atherosclerosis. However, the biological mechanisms remain little explored. wrote researchers from Peking University (China) in a study published in the journal Journal of the American College of Cardiology.
210 young people exposed to high ozone concentrations were monitored
This is why, as part of this work, they were interested in the associations between short-term exposure to ozone, hypoxia (i.e. insufficient oxygen supply to meet the body’s needs ) which is recognized as an essential factor in cardiovascular diseases linked to ozone, and arterial stiffness. To carry it out, the team recruited 210 healthy young people living in two cities located at different altitudes on China’s Qinghai-Tibetan Plateau, where ozone concentrations are high and particle pollution is low.
Participants had four medical visits to assess ambient ozone exposure levels, hypoxic biomarkers, and arterial stiffness. “We further examined the modification of the effect by altitude of residence and the robustness of the results to including PM2.5 (particles ≤2.5 μm aerodynamic diameter) in two-pollutant models,” the scientists predicted.
-Ozone exposure linked to hypoxia and arterial stiffness
Ozone exposure one to seven days before visits was significantly associated with changes in multiple hypoxic biomarkers. An increase of 10 ppb (number of molecules of the gas in question per billion molecules of air) in O3 exposure was linked to significant decreases in oxygen saturation and increases in the number of red blood cells, hemoglobin concentration and hematocrit, with maximum changes of – 0.42%, 0.92%, 0.97% and 1.92%, respectively.
Laboratory analysis of mRNA and protein markers consistently indicated that O3 exposure activated the hypoxia-inducible factor-1 (HIF-1) signaling pathway. According to the authors, a 10 ppb increase in O3 corresponded to a 1.04% to 1.33% increase in carotid-femoral pulse wave velocity, indicating an increase in arterial stiffness. “Increases in red blood cell concentration, hemoglobin, and hematocrit played a significant role in the O3-carotid-femoral pulse wave velocity association, whereas reductions in oxygen saturation did not. had no significant mediating effect.”
“This study uniquely isolates the effects of ozone from other pollutants, providing a critical advance in understanding its independent role in cardiovascular damage,” the researchers concluded.
