Pollution and Cardiac Health

Pollution is epidemiologically associated with higher chances of heart disease. Indeed, long term exposure to the elevated particulate matter levels in pollution is linked to an increased risk of cardiovascular disease mortality for individuals with or without existing cardiometabolic disorders. Reactive Oxygen Species (ROS) assay has been used for evaluating the effect of pollution on cells. To assess the ramifications of pollution on cardiac health in vitro, and the mechanism through which it impacts the cells, ROS assay can be applied to cells that originate in the heart, i.e. cardiomyocytes and cardiac fibroblasts. We hypothesize that the more active cells, cardiomyocytes, will have a greater ROS response to pollution, which is indicative of the functional cardiac response to the presence of pollution. To determine this, cardiomyocytes and cardiac fibroblasts were isolated from neonatal rats. The ROS assay used is a multi-step chemical assay that allows us to quantify the amount of ROS produced in cells after being exposed to pollution. Here the assay is performed on isolated cardiac fibroblasts in addition to a co-culture of both cell types. Heart chip devices are also made to measure contractile strength of cardiomyocytes. This assay uses muscular thin film technology on engineered cardiac tissue to determine contractility after being treated with pollution. Results indicate a higher presence of ROS in cardiomyocytes as opposed to fibroblasts. This is qualitatively illustrated in immunostained co-cultures of both cell types. The lower amount of ROS in the fibroblasts implies that the higher activity (i.e. contraction) of cardiomyocytes causes them to generate more ROS, which might suggest that their function is affected. In order to verify that ROS and cardiac function are correlated, the heart chip device was adapted to study pollution. We have demonstrated that various cells in the heart have different responses to pollution. This illustrates the importance of studying the cardiomyocyte’s functional response to pollution instead of assuming that it correlates with other data.