You are here

Air Pollution and Cardiovascular Diseases

Evidence from numerous clinical studies 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. Research presented at the 2013 Acute Cardiac Care Congress 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 in JAMA. 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.


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.

7. European Society of Cardiology Press Office. Cold weather produces more heart attacks 2013.

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.

10. Krishnan RM, Sullivan JH, Carlsten C, et al. A randomized cross-over study of inhalation of diesel exhaust, hematological indices, and endothelial markers in humans. Particle and fibre toxicology. 2013;10:7.

11. Kotb M, Ramadan H, Motaweh H, Shehata R, El-Bassiouni E. Changes in some biophysical and biochemical parameters in blood and urine of workers chronically exposed to benzene. European Scientific Journal. 2013;9(24).


Stay Connected