For the first time, a team of researchers from the Université libre de Bruxelles (Belgium) has demonstrated a direct link between exposure to a pollutant gas and atherosclerosis in a living being. These works, published in the Journal of Biological Chemistry, highlight the impact of hydrocyanic acid on proteins circulating in the blood and their accumulation in atheromatous plaques.
It is known that air pollution has a major impact on health, including the increased risk of cardiovascular disease. But how do these pollutants actually act on our body? For the first time, a team of researchers from the Université libre de Bruxelles demonstrates a direct link between exposure to a pollutant gas and atherosclerosis in a living being.
The ULB researchers — including Karim Zouaoui Boudjeltia from the Laboratory of Experimental Medicine, Cédric Delporte and Pierre Van Antwerpen from the Analytical Platform of the Faculty of Pharmacy — focused on the metabolisation of hydrogen acid, the volatile form of cyanide. It is one of the unregulated gaseous pollutants, which is generated by the combustion of organic matter resulting from the use of heat engines, the consumption of tobacco, fires, etc. It is therefore not part of the gases measured during the assessment of air quality such as nitrogen dioxide or ozone.
The researchers first demonstrated that a human protein involved in the development of atherosclerosis, myeloperoxidase, is able to oxidize this cyanide by various direct and indirect chemical mechanisms, which promotes transformation of proteins circulating in the blood. With the help of Austrian and American teams, they then injected cyanide into a mouse. This experiment shows that exposure to cyanide induces the accumulation of proteins modified by this pollutant specifically in atheromatous plaques — these plaques that are found in the vessel wall, causing certain cardiovascular diseases. Proteins modified in this way are also involved in triggering inflammatory mechanisms that may become chronic.
Although the implication of protein transformations by myeloperoxidase in cardiovascular disease is well known, pollutant gases have not been involved so far. This is the first time that a direct link between exposure to a pollutant gas and atherosclerosis has been found in a living being. This underlines, if it was still necessary, the role of air pollution in the occurrence of cardiovascular events mediated by atherosclerosis.