Tiny pollution particles produced by vehicle engines and industry are known to worsen heart disease and raise the risk of stroke, but a new study suggests they might also be planting the seeds for cardiovascular disease early on.
In healthy young adults with no signs of heart disease, researchers found that exposure to fine pollution particles known as PM 2.5 led to inflammation-causing changes in immune cells and a rise in debris in the bloodstream representing dead endothelial cells, the type that line blood vessel walls.
Fine particles in the air from industrial pollution and traffic have been tied to heart events, like stroke, before, but most focus has been on older people, said Dr. Joel Kaufman of the University of Washington School of Public Health in Seattle, who was not part of the new study.
“What we’re learning is these air pollution exposures are triggering biologically relevant pathways that we can measure in the blood,” Kaufman told Reuters Health.
“Blood vessel damage is an underlying characteristic of much cardiovascular disease including coronary artery disease and cerebrovascular disease and can lead to serious, even life threatening acute disease events including heart attacks and strokes,” said lead author Dr. C. Arden Pope III of Brigham Young University in Provo, Utah.
“There is substantial epidemiological evidence that long-term exposure to air pollution increases the risk of these events and even of dying of cardiovascular disease,” Pope told Reuters Health.
To see whether and how the fine particles directly affect the cardiovascular system, the researchers collected blood samples from three groups of 24 young, healthy nonsmoking adults each, over three periods between December 2014 and April 2015.
The study team examined samples collected when particle pollution levels were low and high in the Provo area, and looked for microparticles and immune cells that indicate cells are breaking down and dying and that the body is mounting some kind of immune response.
When PM 2.5 pollution levels were higher, blood samples contained more pieces of dead cells from the linings of arteries, veins and lungs. At the same time, levels of factors related to blood vessel growth dipped, and immune-system chemicals that ignite inflammation rose, according to the report in Circulation Research.
Because the participants were healthy and without existing heart disease, the results show that fine particle pollution doesn’t merely aggravate existing cardiovascular problems, the study authors conclude, it may play a part in initiating them.
The new results fill in some of the missing information regarding how breathing air pollution can contribute to not only lung disease, but also cardiovascular disease, Pope said.
In the US, pollution levels have been significantly reduced and it’s something of a success story, Kaufman said, but in other areas of the world particulate pollution hasn’t been addressed. In the US, especially vulnerable people like those who have had a stroke, smokers, people with diabetes or high blood pressure, may need to take extra precautions on high pollution days.
“Air pollution levels encountered even today are capable of having a discernable negative influence on the health of healthy adults beyond impacting just the lungs,” said Dr. Robert D. Brook of the University of Michigan Health System in Ann Arbor, who was not part of the study.
“Cardiovascular disease continues to be a major cause of death and disease,” and blood vessel damage may underlie much of that, Pope said. “We need to continue our public policy efforts to reduce air pollution in our cities and other environments.”