Pneumonia is the leading cause of death among children, killing approximately 2,400 children a day. India recorded the highest pneumonia deaths in the world in the year 2015 of which 1.8 lakhs were children under the age of 5.
There are several reasonable biological mechanisms by which pollution could increase pneumonia risk, for example, increased oxidative stress, impaired immune response, the outburst of the inflammatory response, etc.
Studies have shown that the exposure to ambient air pollutants like nitrogen dioxide, tobacco smoke, biomass fuel smoke, etc. increases susceptibility to respiratory tract infections.
This article discusses how air pollution is responsible for the onset as well as the prevalence of pneumonia.
What is Air Pollution?
Air pollution occurs when harmful or excessive quantities of substances like gases, liquid aerosols, and biological molecules are introduced into the earth’s atmosphere.
Air pollutants of extremely small solid or liquid particles called “particulates” for example, soot, dust, smokes, fumes, mists, etc.
Particulates that are 2.5 to 10 micrometres (μm) in size, also termed as PM10 are significant air pollutants because of their very harmful effects on human health.
They are mostly emitted by various industrial processes, coal- or oil-burning power plants, residential heating systems, and automobiles. Lead fumes, Ozone, and other toxic chemical gases like NO2, SO2, etc. airborne particulates less than 0.5 μm in size are particularly toxic.
What is Pneumonia?
Pneumonia is an inflammatory disease in one or both lungs caused mainly due to bacteria, viruses, or fungi infection and recently by environmental factors like air pollution and toxins. Bacterial pneumonia is the most common type in adults.
The infection causes inflammation in the air sacs of the lungs, which are called alveoli. The air sacs in the lung tissue (alveoli) fill with fluid or pus, making it difficult to breathe.
Pneumonia although it is a lung disorder, severe complications can lead to problems in other parts of the body, too. These can be very serious and even deadly.
The link between Air pollution and Pneumonia
Research has proven a definitive link between air pollution and pneumonia. Air pollution is known to cause oxidative stress which can not only lead to worsening of existing pneumonia condition but also in some cases development of pneumonia. Air pollution also causes inflammation damaging effects on the epithelial cell lining. leading to other issues such as pulmonary oedema, coagulation of blood, and cell death in lung tissue.
These are further discussed in detail in coming sections –
Oxidative stress due to air pollution can cause or aggravate pneumonia
The lung is exposed to several thousand litres of air per day and every breath carries with it a very large number of compounds with oxidative potential, including air pollution, pollen, and particulate matter.
Although larger particles are efficiently filtered out by the nose and upper airways, fine particles can easily access the lower airways and promote increased airway oxidation and inflammation.
Air pollutants such as ozone, particulate matter, and nitrogen dioxide have been shown to induce lung inflammation through stimulation of the oxidative stress process.
Respiratory tract lining fluids (RTLFs) is a thin layer of fluid which covers the epithelial surface of the respiratory tract. It comprises of anti-oxidants and is apparently the first line of defense in the respiratory tract.
Once the ozone (O3) comes into contact with the RTLFs, it induces oxidative stress by two different mechanisms. The first one is by reacting directly with the constituents of the RTLF and the underlying epithelium cell lining.
The second mechanism is an indirect reaction because, even though O3 does not react directly with the epithelial cells, these cells do react in response to the oxidation products produced in the RTLF.
As a consequence, they release a variety of pro-inflammatory mediators and more reactive oxygen species (ROS).
Another major risk factor contributing to the oxidative stress in the respiratory tract is the traffic-related fuel emission. Traffic-related air pollutants contain both toxic gases and various particulate matters (PMs).
These PMs and gases are made up of various chemical composition and hence it is likely to induce either a direct or indirect oxidation process when they come in contact with the RTLFs.
All these processes together could overthrow the existing anti-oxidant network leading to an increase in the oxidative process.
The intensity of which varies depending on the amount of air pollution inhaled and also on the antioxidants present in the RTLFs.
If the oxidative stress is sufficient, the activation of an inflammatory response occurs and is characterized by the increase and activation of pro-inflammatory molecules like neutrophils.
These neutrophils further induce the rapid release of reactive oxygen species this process is termed as the “respiratory burst process”. Hence, the overproduction of ROS might result in oxidative stress in the airway tissues.
Oxidative stress can have negative effects on proteins, lipids, carbohydrates, RNA, and DNA that are the main components of cells. It throws the cells into a negative cascade of the process that can eventually lead to cell dysfunction and cell death.
Oxidative stress can occur from a number of sources, including ozone, traffic-exhaust, indoor pollution, etc. Airway oxidative stress is a complex phenomenon with important functional and biological effects in both developing and progression of pneumonia.
Air pollution causes inflammation of the lung tissue in pneumonia
Inhalation of air pollution has been shown to stimulate respiratory tract inflammation due to its oxidative nature. The oxidative process that triggers an inflammatory response due to its damaging effects on the epithelial cell lining.
Alternatively, ultra-fine particulate matter (PM2.5, diameter < 2.5 μm) can react with the respiratory epithelium cells and promote subsequent, release of pro-inflammatory molecules, namely cytokines.
Airway inflammation can lead to the destruction of the cilia of the epithelial cells that line the respiratory tract.
The cilia have an important immune function because they constantly move the mucus up from the lungs to the back of the throat where it is eliminated or swallowed and digested.
The mucus serves as a “trap” for infectious agents and small particles, such as pollutants and allergens, preventing them to enter deep into the airways and lungs.
Another consequence of airway inflammation is lung epithelial injury which leads to an open crossing point between the lung and the blood.
This facilitates the spreading of microbes to the rest of the body, initiating a universal inflammatory response.
If the lung epithelial injury is chronic and the tissue is frequently going through a repairing process, this can lead to the formation of scars in the lung tissues (alveoli), which leads the decrease in lung function, chest discomfort, fatigue, and weakness.
“Pulmonary oedema” is commonly associated with pneumonia, it literally means an excess collection of watery fluid in the lung.
Due to lung epithelial injury and the resulting chronic inflammatory response, it leads to leaky alveoli that can fill up with fluid from the blood vessels.
Inflammation occurring at a single site causes white cells (leukocyte) activation and release of numerous cytokines, oxygen metabolites, and other mediators of inflammation.
These inflammatory mediators may trigger the activation of coagulation cascades as well.
This coagulation of blood in the lungs further lead to decreased lung function, and thickened alveoli air sacs.
A bi-directional relationship between coagulation and inflammation appears to play a pivotal role in the mechanisms leading to organ failure in patients with severe pneumonia.
In several studies, it has been shown that short-term exposures to diesel exhaust have caused respiratory inflammation both in animals and humans.
For example, in a study conducted in London, adults with asthma showed a decreased lung function and increased lung inflammation markers after a 2 hours walk on Oxford Street, a heavy diesel traffic area, compared to a walk in the Hyde Park.
Inhalation of air pollution has been shown to stimulate airway inflammation due to its oxidative nature. Inflammatory response leads to oxidative stress, pulmonary oedema, coagulation of blood, and cell death in lung tissue.
There are reasonable biological mechanisms by which pollution could increase the risk of pneumonia.
Population-based studies indicate that hospitalizations for respiratory causes are strongly related to PM exposure.
Researchers hypotheses several possible underlying mechanisms in the development and progression of pneumonia.
Studies have shown that high doses of particles can trigger oxidative stress and the initiation of inflammation, increased blood coagulation, impaired cellular defence, and modulation of the immune system.
Chronic effects may also arise from the repeated cycles of lung cell injury and repair. For example, some particles can cause epithelial cell damage, pulmonary oedema, and eventually cell death.
To reduce the damaging effects of air pollution, people especially those with pneumonia or asthma should be aware of the air quality.
It is highly advisable to take extra measures such as reducing the time outdoor and wearing masks when necessary.
Whereas for reducing the air pollutants indoor, people should use clean fuels and improve the stoves so as to burn fuel more efficiently and have a proper ventilation system. Air purifiers that can help improve the air quality efficiently are also recommended.