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 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.
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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 U.S., 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
U.S., 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.”
SOURCE: http://bit.ly/2dUgPL1 Circulation Research, online October
25, 2016.
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