Air pollution is the presence of unwanted and harmful substances such as chemicals, dust, auto emissions, suspended particles, gases among others in our atmosphere.
Air pollution is a serious threat to the health of living beings and the different ecosystems found in our environment.
According to WHO, it was the cause of death of approximately 7 million people around the world in 2014.
There are accumulating evidence indicate that air pollutants contribute to serious, even fatal damage to the cardiovascular system. North India suffers from heavy winter smog every year due to its toxic air quality.
The particulate pollutants PM2.5 are the main cause of reduced visibility are suspended particles in either medium like gaseous or liquid.
Table of Contents
What is Coronary Artery Disease (CAD)?
Coronary artery disease (CAD) also known as Ischemic Heart Disease (IHD) or “hardening of the arteries.”
It refers to the group of heart conditions caused due to narrowing of heart arteries or build-up in the arteries and causes “ischemia,” which means the heart is not getting enough blood flow and oxygen.
Studies suggest that CAD starts when certain factors damage the inner layers of the coronary arteries.
The build-up of plaque narrows the coronary arteries and reduces the flow of oxygen-rich blood to the heart.
Relationship between Coronary Artery Disease and Air pollution
The number of studies shows a strong link between the PM and the deaths caused due to cardiovascular diseases, and several pathways have recognized that can explain the link between PM particles and cardiovascular diseases.
The first is the direct pathway where, PM2.5, in particular, Ultra-Fine Particles (UFPs) directly translocate into the bloodstream and remote target organ. For the indirect pathways, the one is mediated by pulmonary oxidative stress and inflammatory response.
These indirect pathways are less acute and occur after several hours or days of inhalation. Interaction on the autonomic nervous system via specific lung receptors is an indirect pathway well documented by many scientists and researchers.
1. Particulate matters enhances coagulation/thrombosis
It has been suggested that air pollutants, especially PM2.5, may induce inflammation, which would increase the concentrations of acute phase reactants like fibrinogen.
Fibrinogen is a glycoprotein responsible for synthesis blood-clots to obstruct blood vessels and thereby stop excessive bleeding.
Fibrinogen is an important risk factor for cardiovascular diseases, especially ischaemic heart disease.
Seaton et al. proposed that inhaled pollutants induce inflammation with release of mediators capable of increasing blood coagulability.
Coagulation factors such as FVII and fibrinogen, which are part of the acute‐phase responses mediated by cytokines released during inflammatory reactions, increase after short‐term exposure to particles.
In large individual participant meta-analysis, moderately strong associations were found between the normal plasma fibrinogen level and the risks of Coronary Heart Disease, stroke, and other vascular mortality, and nonvascular mortality in a wide range of circumstances in healthy middle-aged adults.
C-reactive proteins are produced by the liver in response to inflammation. CRP concentration has continuous associations with the risk of coronary heart disease, ischaemic stroke, vascular mortality, and death from several cancers and lung disease.
The relevance of CRP to such a range of disorders is unclear. Associations with ischaemic vascular disease depend considerably on other conventional risk factors and other markers of inflammation.
Particulate matters (PM2.5 and PM10) when comes in contact with blood enhance inflammation that triggers the production of various coagulants.
2. Acute arterial vasoconstriction
Vasoconstriction is the narrowing of the blood vessels resulting from contraction of the muscular wall of the vessels, in particular, the large arteries and small arterioles.
Fine particulate air pollution and ozone are associated with increased cardiovascular events.
Traffic-related air pollution is consistently associated with cardiovascular morbidity and mortality.
Recent human and animal studies suggest that exposure to air pollutants affects vascular function.
Diesel exhaust (DE) is a major source of traffic-related air pollution.
Researchers hypothesized that PM may activate the angiotensin type 1 receptor (AT1R), a protein-coupled receptor that regulates inflammation and vascular function.
Inhalation of concentrated ambient air particles (CAPs) (~ 150 μg/m3) and ozone (120 ppb) for 2 hours causes acute constriction of the brachial artery in healthy adults.
In a study, conducted using healthy rats and rats suffering from chronic bronchitis were exposed to CAPs for three consecutive days.
The results indicate that short-term CAPs exposures can induce vasoconstriction of small pulmonary arteries in both normal and CB rats.
In another study involving healthy humans, exposure to dilute diesel exhaust promotes myocardial ischemia and inhibits endogenous fibrinolytic capacity in men with stable coronary heart disease.
Our findings point to ischemic and thrombotic mechanisms that may explain in part the observation that exposure to combustion-derived air pollution is associated with adverse cardiovascular events.
Inhalation of concentrated ambient air particles and ozone for 2 hours causes acute constriction of the arteries in healthy adults.
3. Systemic Inflammatory Response Syndrome (SIRS)
It is an inflammatory state, the body’s response to an infectious or non-infectious abuse. It is a known fact that inflammation and coronary heart disease are strongly interconnected and mutually reinforce each other.
Particulate matters stimulate alveolar macrophages (AM- type of immune cells present in the lung) to produce pro-inflammatory cytokines and these cytokines are also found in the blood.
Hence, scientists postulate that these cytokines induced a systemic inflammatory response that has an important role in the pathogenesis of the cardiovascular adverse health effects associated with atmospheric pollution.
Another hypothesis suggests that suggest that the deposition of PM on epithelial cells that line the airways activates inflammatory signaling cascades.
Some of the dangerous pollutants get into the atmosphere naturally from forest fires, lightning strikes, and erupting volcanoes, but most of these pollutants are put into the atmosphere by humans.
Anthropogenic (man-made) sources include combustion within car engines, solid-fuel combustion in households, industrial activities (such as building, mining, manufacturing of cement, ceramics, and bricks, and smelting), quarrying, and mining.
In a study, healthy mice were exposed to PM2.5 or filtered air for 5, 14, and 21 days, respectively. PM2.5 exposed mice demonstrated a significant inflammatory response after 5 days of exposure in the lung tissue and broncho-alveolar lavage fluid.
These findings suggest that PM2.5 exposure induces the inflammatory responses from both macrophages and neutrophils involvement.
Researchers hypothesise that the deposition of PM on epithelial cells that line the airways activates inflammatory signalling cascades.
Atherosclerosis is the narrowing of arteries due to plaque build-up on the artery walls.
There are many studies both in human and animals suggesting that air pollution causes atherosclerosis.
Increased concentrations of PM2.5 and traffic-related air pollution within metropolitan areas worldwide are associated with progression in coronary calcification, consistent with the acceleration of atherosclerosis.
In a meta-analysis conducted by MESA in 2013 showed that higher long-term PM2.5 concentrations are associated with increased intima-medial thickness (IMT- measures the thickness of the inner two layers of the carotid artery) progression and that greater reductions in PM2.5 are related to slower IMT progression.
Interestingly, the MESA Air study also found that improvements in air quality were linked to slower IMT progression.
Other investigators have shown that similar changes in human atherosclerotic plaques indicate abrasions that are more vulnerable to rupture, with hemorrhage into the plaque, thrombotic constriction of the artery and development of an acute coronary syndrome.
When this plaque ruptures, blood cell fragments called platelets stick to the site of the injury and may clump together to form blood clots. Blood clots can further narrow the coronary arteries and worsen angina.
If a clot becomes large enough, it can mostly or completely block a coronary artery and cause a heart attack.
Most recently, researchers funded by EPA’s STAR grant program at the University of Washington completed the Multi-Ethnic Study of Atherosclerosis Air Pollution Study (MESA Air), a decade-long study that reveals a direct link between air pollution and atherosclerosis, which is a build-up of plaque in the coronary artery that can affect heart health.
Chronic inhalation of air pollutants not only causes atherosclerosis but promote the progression and vulnerability of atherosclerotic plaques. The air particulates anchor themselves in the arteries and induce a series of cascades leading to its build-up.
5. Oxidative stress
Oxidative stress is an imbalance between free radicals and antioxidants in your body. The mechanisms of air pollution-induced health effects involve oxidative stress and inflammation.
There is overwhelming evidence from animal experimental models, cell culture experiments, and cell-free systems that exposure to diesel exhaust and diesel exhaust particles causes oxidative DNA damage.
Similarly, various preparations of ambient air PM induce oxidative DNA damage in vitro (in-glass) systems, whereas in vivo (in living being) studies are rare.
Another experimental evidence has revealed a possible biological mechanisms pathway involves the initiation of pulmonary and systemic oxidative stress and inflammation by components within PM.
Subsequently, a cascade of physiological responses may follow that are capable of instigating cardiovascular events.
These include alterations in blood flow that favour thrombosis, cardiac dysrhythmias, acute vascular dysfunction, plaque instability, and the long-term development of atherosclerosis.
Oxidative stress-induced DNA damage appears to be an important mechanism of action of urban particulate air pollution leading to a series of coronary and pulmonary health defects.
Research and various studies evidence that both short-term and long-term exposure to air pollution is a cardiovascular disease risk factor that should be taken seriously.
In addition to encouraging policy-makers to consider the long-term impacts of low levels of air particle pollution and motivating healthcare providers to learn more about the effects of air pollution on the cardiovascular system, it also emphasizes the importance of monitoring air quality to protect heart health.
Long-term improvements in air pollution have shown to reduce mortality rates. For example, reductions in PM2.5 concentration in 51 metropolitan areas were correlated with significant increases in life expectancy.