Most of us know that smoking is harmful to our lungs. Have you ever thought of how inhaling smoke particles over a long period of time will damage our lungs? Or even wondered why heavy smokers had difficulty in breathing when they get flu.

In Emphysema, one of the respiratory diseases found in smokers, the lung tissue gets damaged due to the smoke particles that get settled in the air sacs of the lung. The air sacs are also called as alveoli (Figure 1), where the gaseous exchange of oxygen and carbon dioxide takes place. So, imagine our alveoli, where a process that is vital to our survival takes place, gets damaged slowly over a period, how much difficult would it be for our body to take in oxygen and give out carbon dioxide.

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Figure 1: Trachea (windpipe) branches out into bronchi, bronchioles and finally alveoli.

When a person smokes, the smoke particles pass through the trachea, bronchi, bronchioles and finally, they reach the alveoli. Defensive mechanisms called cilia lines the trachea to the bronchi. Imagine the cilia as the police officers of the lung.  The cilia have a brush-like appearance that has the capability to sweep up the dust particles, thereby protecting the lung. Though the cilia are present, it has no defensive role against the smoke particles. This is because the smoke particles have a very small size that it can escape the action of cilia. So, when the police officers fail to defend, the next defensive system would be an army of soldiers. The soldiers in our lung are macrophages and neutrophils.

Once the smoke particles reach the alveoli, macrophages will get alerted and signal the neutrophils from the blood vessels to come to the site. Macrophages and neutrophils are white blood cells that play a major role in eliminating anything that has damaging effects on our body. They will produce some enzymes called proteases to remove the smoke particles through a chemical attack. Since proteases have a very strong ability to cause destruction even to the lung tissue, the lungs produce some enzymes called antiproteases. Antiproteases protects the body from the attack by proteases. In a normal condition, the lungs always maintain an equal number of protease and antiprotease production. Prolonged exposure of the alveoli to the smoke particles, mainly in heavy smokers, may lead to an increased production of proteases. When the number of proteases increases, the number of antiproteases produced will decrease relatively. Therefore, this unbalanced ratio will lead to damage in alveoli.

Alveoli are elastic in nature. When air is breathed in, the alveoli inflate (like a balloon). When air is breathed out, the alveoli recoil. In emphysema, the elasticity of the alveoli is lost because of the protease activity. Therefore, when the air is breathed in, there is too much inflation. Also, there is difficulty to breathe out due to poor recoil capability. Hence, heavy smokers have breathing problems and very severe coughs to breath out completely.


Sharafkhaneh, A., Hanania, N. A. & Kim, V., 2008 . Pathogenesis of Emphysema. PROCEEDINGS OF THE AMERICAN THORACIC SOCIETY, [Online]. 5(4), p. 475–477. Available at: [Accessed 23 June 2018].

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