By Joseph Weidman, November 13, 2013
Research presented at the Acute Cardiac Care Congress 2013 annual meeting has linked air pollution with increased heart attacks.1 An
increasingly important environmental and health issue, air pollution is
an established cause of respiratory diseases, however its connection
with cardiovascular diseases is not as well-known. The research,
presented by Savina Nodari from Brescia, Italy, measured general air
pollution as levels of particulates having diameters of 10 micrometers
or less (PM-10). PM-10 and daily hospitalizations for cardiac events
were recorded in Brescia, Italy from 2004 to 2007. This region of
northern Italy has shown higher average daily PM-10 levels than the 50
micrograms/m3 safety threshold set by the European Environmental Agency.
Direct Link Between Pollution and Heart Risk
The study found a significant linear relationship between PM-10 levels
and acute cardiovascular events (acute coronary syndrome, atrial
fibrillation and ventricular arrhythmias, and acute heart failure).
Each 10 microgram/m3 increase in PM-10 was responsible for a 3% increase in cardiovascular event admissions.
Nodari, a cardiologist, highlighted previous studies showing that,
“PM-10 can induce processes that are bad for the heart including
inflammation and coagulation”.1 Previously,
a 2010 statement from the American Heart Association indicated that PM
< 2.5 microns can trigger cardiovascular disease-related morbidity
and mortality after just hours to weeks of exposure.2 Furthermore,
exposure over a few years increases these risks to a greater extent,
while reduction of particulate matter decreases cardiovascular mortality
within a few years.
Broad Evidence-Based Support
The results of this study are supported by findings of a 2012 meta-analysis published inJAMA.
This analysis of 34 clinical studies found that the relative risk of
myocardial infarction was significantly increased with short-term
exposure (up to 7 days) of carbon monoxide, nitrogen dioxide, sulfur
dioxide, PM-10, and PM-2.5.3 The
authors of this study suggested that air pollution may increase
systemic inflammation, dysregulation of autonomic cardiac function, and
blood viscosity. They underscored that elevated blood viscosity can
increase clotting risk, accelerate advancement of atherosclerosis, and
destabilize atherosclerotic plaques.
Air pollution,4 like whole blood viscosity and vulnerable low wall shear stress,5,6 is linked to intima-medial thickness progression, a marker of atherosclerosis development.
These studies join a plethora of scientific research that examine the
impact of environmental factors on human health. A Belgium study
presented at the European Society of Cardiology Congress 2013
investigated various environmental triggers for acute myocardial
infarction (AMI) in about 16,000 individuals. Air pollution
measurements included PM-10, PM-2.5, and black smoke, all of which were
positively correlated to AMI when looked at individually.7
A multivariate analysis found these results did not reach significance,
however, environmental temperature had a significant negative
correlation with AMI, showing a 7% increase in odds ratio for every 10°C
temperature decrease. The meta-analysis concluded that temperature,
when compared to other environmental factors, may have the most profound
effect on triggering AMI.
One of the study’s researchers, Belgian cardiologist Marc Claeys, suggested increased blood viscosity as a potential mechanism for cold temperatures triggering AMI.
Interestingly, thicker blood may also mechanistically explain the
increased cardiovascular risks tied to air pollution in many other
studies.
Is Blood Viscosity a Possible Mechanism Mediating the Cardiovascular Risk of Pollution?
Short exposures to high levels of PM-10 have been shown to increase
systemic inflammatory markers which are directly related to endothelial
dysfunction, an early initiator of atherosclerotic plaque development.8 A
cross-sectional analysis of 3,256 men and women aged 25-64 years
validated this hypothesis during a 1985 air pollution episode throughout
western and central Europe. After adjusting for traditional
cardiovascular risk factors and other environmental factors, plasma
viscosity was significantly elevated during the air pollution episode.
Plasma viscosity, a major determinant of whole blood viscosity, has been
positively associated with myocardial infarction, stroke, and stroke
severity in other studies.9 Additionally,
heart rate elevation in response to air pollution was shown to be
significantly higher in those with higher blood viscosity.9 This suggests a physiologic adaptation to a hypoxic state where thick blood is unable to efficiently deliver oxygen to cells.
A small 2013 study of traffic-related air pollution, which is a
recognized trigger for acute cardiovascular events, helps to elucidate
these findings. The study demonstrated hemoconcentration and
thrombocytosis, both contributors to elevated blood viscosity, as a
result of short-term diesel exhaust exposure. Other inflammatory
mediators did not show significant increases.10
Separately, a study of 330 individuals showed that occupational benzene
exposure, a product of petroleum, increased relative blood viscosity by
94% when compared with healthy controls, despite significant hemolysis.11 These results were likely due to increased inflammatory markers and oxidative stress.
With rapid industrialization in developing nations and cardiovascular
diseases already remain the number one cause of mortality worldwide,
any improvement in air pollution regulations and new technologies to
reduce air pollution can result in substantial health economic
benefits. Air pollution may be particularly detrimental to those with
elevated baseline blood viscosity.
Polluted air has the potential to elevate blood viscosity and increase
cardiovascular risk by inducing an inflammatory, oxidative, and stressed
physiologic state. Specifically, changes in red blood cell morphology,
plasma proteins, and red blood cell concentration may all contribute to
pollution-induced hyperviscosity.
References
1. European
Society of Cardiology Press Office. Air pollution increases heart
attacks: Men, older people and patients with a previous CV
hospitalisation are at greater risk. 2013.
2. Brook
RD, Rajagopalan S, Pope CA, 3rd, et al. Particulate matter air
pollution and cardiovascular disease: An update to the scientific
statement from the American Heart Association. Circulation. Jun 1 2010;121(21):2331-2378.
3. Mustafić H, Jabre P, Caussin C, et al. Main air pollutants and myocardial infarction. JAMA: the journal of the American Medical Association. 2012;307(7):713-721.
4. Adar
SD, Sheppard L, Vedal S, et al. Fine particulate air pollution and the
progression of carotid intima-medial thickness: a prospective cohort
study from the multi-ethnic study of atherosclerosis and air pollution. PLoS medicine. 2013;10(4):e1001430.
5. Lee
AJ, Mowbray PI, Lowe GD, Rumley A, Fowkes FGR, Allan PL. Blood
viscosity and elevated carotid intima-media thickness in men and women:
the Edinburgh Artery Study.Circulation. 1998;97(15):1467-1473.
6. Gnasso
A, Carallo C, Irace C, et al. Association between intima-media
thickness and wall shear stress in common carotid arteries in healthy
male subjects. Circulation. Dec 15 1996;94(12):3257-3262.
8. Mills NL, Tornqvist H, Robinson SD, et al. Air pollution and atherothrombosis. Inhalation toxicology. 2007;19 Suppl 1:81-89.
9. Peters A, Doring A, Wichmann HE, Koenig W. Increased plasma viscosity during an air pollution episode: a link to mortality? Lancet. May 31 1997;349(9065):1582-1587.