Luchtvervuiling veroorzaakt hart- en vaatziektes.*
Luchtvervuiling
kan bijdragen aan de ontwikkeling van hart- en vaatziekten, blijkt uit een
Amerikaans onderzoek met muizen.
De onderzoekers maakten gebruik van muizen die genetisch waren gemodificeerd
zodat ze vatbaarder waren voor hart- en vaatziekten. Eén groep muizen
kreeg vervuilde lucht in te ademen, vergelijkbaar met de lucht in New York.
Een andere groep ademde gefilterde lucht. De helft van beide groepen werd
bovendien op een vetrijk dieet gezet. De andere helft kreeg een normale
hoeveelheid vet in de voeding.
Na een half jaar bleken alle muizen die de vervuilde lucht hadden
ingeademd - zowel degene die op een vetrijk dieet stonden als degene die
normaal voedsel kregen - meer cholesterol in hun bloed te hebben dan de
muizen die schone lucht hadden ingeademd. Bij de muizen in de subgroep die
op een normaal dieet stond en vervuilde lucht ademde, was de aorta voor
19,2% met vetachtige substanties dichtgeslibd. Bij de muizen met een
normaal dieet en gefilterde lucht was dat 13,2%. Bij de muizen die vetrijk
voedsel kregen en vervuilde lucht inademden, was het 41,5% en bij de
muizen met een vetrijk dieet en gezuiverde lucht 26,2%. Het
onderzoek werd uitgevoerd aan de medische faculteit van de Universiteit van
New York.
De
resultaten werden gepubliceerd in het Journal of the American Medical
Association (JAMA). "We
hebben hiermee een oorzakelijk verband aangetoond tussen luchtvervuiling en
atherosclerose", aldus Dr. Lung chi Chen, docent in milieugeneeskunde
aan de Universiteit van New York. Atherosclerose is een veel voorkomende
ziekte waarbij vetachtige stoffen in de wand van slagaders worden afgezet.
De bloeddoorstroming wordt daardoor gehinderd.
How
Can Air Pollution Cause Heart Disease? New York University School Of Medicine
New York University School of
Medicine researchers provide some of the most compelling evidence yet that
long-term exposure to air pollution--even at levels within federal standards--causes
heart disease. Previous studies have linked air pollution to cardiovascular
disease but until now it was poorly understood how pollution damaged the body's
blood vessels.
In a well-designed mouse study, where animals breathed air as polluted as the
air in New York City, the researchers pinpointed specific mechanisms and showed
that air pollution can be particularly damaging when coupled with a high-fat
diet, according to new research published in the December 21 issue of JAMA.
"We established a causal link between air pollution and atherosclerosis,"
says Lung Chi Chen, Ph.D., Associate Professor of Environmental Medicine at NYU
School of Medicine and a lead author of the study. Atherosclerosis--the
hardening, narrowing, and clogging of the arteries--is an important component of
cardiovascular disease.
The study, done in collaboration with the Mount Sinai School of Medicine and
University of Michigan, looked at the effects of airborne particles measuring
less than 2.5 microns, referred to as PM2.5, the size linked most strongly with
cardiovascular disease. The emissions arise primarily from power plants and
vehicle exhaust. The US Environmental Protection Agency (EPA) has regulated
PM2.5 since 1997, limiting each person's average exposure per year to no more
than 15 micrograms per cubic meter. These tiny particles of dust, soot, and
smoke lead to an estimated 60,000 premature deaths every year in the United
States.
Dr. Chen and his colleagues divided 28 mice, which were genetically prone to
developing cardiovascular disease, into two groups eating either normal or
high-fat diets. For the next six months, half of the mice in each feeding group
breathed doses of either particle-free filtered air or concentrated air
containing PM2.5 at levels that averaged out to 15.2 micrograms per cubic meter.
This amount is within the range of annual EPA limits and equivalent to air
quality in urban areas such as New York City.
The researchers then conducted an array of tests to measure whether the PM2.5
exposure had any impact on the mice's cardiovascular health. Overall, mice who
breathed polluted air fared worse than those inhaling filtered air. But when
coupled with a high-fat diet, the impact of PM2.5 exposure was even more
dramatic. The results added up to a clear cause and effect relationship between
PM2.5 exposure and atherosclerosis, according to the study.
On the whole, mice breathing polluted air had far more plaque than those
breathing filtered air. In cross sections taken from the largest artery in the
body--the aorta--mice on normal diets and exposed to PM2.5 had arteries 19.2
percent filled with plaque, the fatty deposits that clog arteries. The arteries
of those breathing particle-free air were 13.2 percent obstructed. Among
high-fat diet mice, those exposed to PM2.5 had arteries that were 41.5 percent
obstructed by plaque, whereas the arteries of the pollution-free mice were 26.2
percent clogged. In both normal and high-fat diet mice, PM2.5 exposure increased
cholesterol levels, which are thought to exacerbate plaque buildup.
Though findings for increased plaque among mice eating normal diets were not
statistically significant, Dr. Chen believes that future research on larger
numbers of animals will solidify the trend. "Even with the low-fat diet,
there's still something there. So that is something to think about," he
says. He suspects that PM2.5 exposure could also greatly affect even people who
do not eat high-fat diets.
Mice exposed to PM2.5 also appeared prone to developing high
blood pressure, another
element of cardiovascular disease, because their arteries had become less
elastic.
To measure tension in the arteries, the researchers tested how the
neurotransmitters serotonin and acetylcholine affected the aortic arches of
PM2.5-exposed mice differently than those of controls. The arteries taken from
exposed mice were less elastic than the control group, constricting more in the
presence of serotonin and relaxing less in response to acetylcholine.
Once again, the mice fed high-fat diets suffered the most pronounced effects
from breathing polluted air.
Finally, the researchers also examined various measures of vascular inflammation,
which is involved in atherosclerosis on a number of levels. In the aortas of
PM2.5-exposed mice, for example, they found increased levels of macrophages,
immune cells that are an important ingredient in plaque deposits and also active
participants in a biochemical pathway related to inflammation. The study
revealed several signs that this pathway was more active, strengthening the
connection between airborne particles and cardiovascular disease.
The authors of the new study are: Morton Lippmann, Lung Chi Chen, and Ximei Jin
of the NYU School of Medicine's Nelson Institute of Environmental Medicine,
based in Tuxdeo, New York; Qinghua Sun, Alex Natanzon, Juan-Gilberto S.
Aguinaldo, Zahi A. Fayad, Valentin Fuster, and Sayjay Rajagopalan of the Mount
Sinai School of Medicine, New York; and Robert D. Brook and Damon Duquaine of
University of Michigan, Ann Arbor. The study was funded by the EPA and the
National Institute of Environmental Health Sciences.
Jennifer Choi
jennifer.choi@nyumc.org
New York University Medical Center and School of Medicine
www.med.nyu.edu
( December 2005)
