Air pollution’s effect on our blood vessels

Is air pollution that bad? Are cardiovascular diseases a big problem?

It’s long been known that air pollution contributes to global warming and can affect our lungs. This article shows us that air pollution may go one step further and actually affect our cardiovascular system too!


The first graph (A) shows the risk factors for diseases leading to death around the world between 1990 and 2015. You can see that high blood pressure is still the biggest risk factor for death around the globe. The second graph (B) shows the number of deaths due to PM2.5. PM2.5 is basically a complicated way of saying very very small particles (smaller than dust or pollen) – take a look at the picture below. Some definitions for graph A: Tracheal and Bronchial refer to the breathing tubes of the lungs (dark blue), Ischaemic means a restriction of blood flow causing less oxygen to be able to get where it’s supposed to go (light blue), Cerebrovascular refers to the blood vessels of the brain (red), Chronic Obstructive Pulmonary Disease, also known as COPD refers to a group of lung conditions that cause trouble breathing (purple) and lower respiratory tract infections are lung infections like Pneumonia (green).

So what we can see here is that clearly deaths due to an increase in PM2.5 pollution are increasing. PM2.5 particles are particularly bad as they can penetrate deep into your lungs when you breathe them in as they’re so small.



What has air pollution got to do with our blood vessels?

This study looked into endothelial cells (or the endothelium part of a blood vessel). These are a thin layer of cells on the inside of our blood vessels that have direct contact with our blood. Whilst pollution has been shown to affect our cardiovascular system in many different ways, one of the critical steps that leads to the risk factors described above are changes to the endothelium. These cells are involved in the constriction or relaxation of our blood vessels (scientists call this vascular tone). They are also important in injury repair.


How do our endothelial cells go wrong?

So now we know that air pollution containing very small particles of pollutants (carbon monoxide, nitrogen dioxide and many others) are increasing the number of PM2.5 related deaths – how does it actually affect our cardiovascular system?

One of the main causes of damage to our blood vessels is through a process called oxidative stress. This process happens when reactive oxygen species are present in our lungs and blood stream. These are highly reactive chemicals (they are also found in bleach and in our own immune system to kill pathogens). These reactive chemicals can damage our blood vessels and mutate our DNA.

This article explains that we have evidence of air pollution causing the production of reactive oxygen species in in vitro cell culture (testing cells in the lab), animal and human studies. Animal studies have also shown that if you remove the mechanism that causes reactive oxygen species (in this case pollution), endothelial and blood vessel health starts to get better. Other studies showed that certain air pollutants can get into the central nervous system (the brain and spinal cord) and affect your blood pressure and metabolism. Our body’s immune system can also become affected as it attempts to clear the pollutants and reactive oxygen species from our body, meaning less availability to fight off infections.

What does this all mean?

Whilst it is widely known that pollution affects our lungs and contributes to global warming, this article has shown that pollution could also affect our blood vessels, metabolism, blood pressure and immune system. This article argues that with the increasing population and life expectancy causing an increase in energy and transportation requirements, more research should be done to protect millions of at risk people from cardiovascular diseases caused by pollution. Pollution’s direct influence on global warming will also have an impact on health as temperatures rise and carbon dioxide levels increase.


Reference: https://academic.oup.com/eurheartj/article/39/38/3543/5074161

Journal: European Heart Journal, Volume 39, Issue 38

Authors: Thomas Münzel, Tommaso Gori, Sadeer Al-Kindi, John Deanfield, Jos Lelieveld, Andreas Daiber and Sanjay Rajagopalan

Copyright: Open Access