A new study published in the journal Environmental International has shown that exposure to microplastics may directly accelerate atherosclerosis, a vascular disease related to plaque buildup and hardening of the artery walls.
The study used mice as a model to better understand the impact of microplastics on the cardiovascular system. The mice were divided into an experimental group and a control group that were fed the same diet. The experimental group of mice were administered microplastics every day for nine weeks, while the control group received a placebo. The amount of microplastics per day in the experimental group was similar to the amounts that may be encountered by humans in contaminated food and water. Over the course of the study, both groups of mice were monitored for the development of atherosclerosis. Exposure to microplastics has been linked to a higher risk of both cardiovascular disease and stroke in humans, and this study aimed to determine how regular exposure to microplastics might impact the cardiovascular system, particularly the veins.
The results showed that male mice who were exposed to microplastics showed a significant increase in rates of atherosclerosis. These mice showed 63% more plaque in the aortic root and an astonishing 624% more plaque in the brachiocephalic artery. Female mice, however, showed no significant changes in plaque buildup during the study. Both groups of mice showed no increases in weight or cholesterol levels, suggesting that changes in plaque buildup were caused by the microplastics themselves rather than other traditional risk factors.
The authors noted that their study is some of the strongest evidence to date suggesting that microplastics may directly cause cardiovascular disease rather than simply being correlated with it. One aspect of the study that remains to be investigated is why males were impacted by microplastics while females were not. More research is needed to determine potential mechanisms behind this effect and to see whether the same effect is present in humans.
Sources: Environmental International, Science Daily
