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Home > Respiratory Health > How Smoking Affects Lung Health

How Smoking Affects Lung Health

October 20, 2020 - Updated on August 11, 2021
5 min read
By Shantanu Singh, MD | Internist  and Nivedita Jha, MBBS

In this article:

  • How Does Smoking Affect Lung Health?
  • Effects of Smoking on the Different Parts of the Lungs
  • Final Word

Smoking is one of the top causes of various diseases, such as lung cancer, chronic obstructive pulmonary disease (COPD), heart disease, and stroke, which can eventually lead to death.

smoking is harmful for lungs

Smoking can affect almost all organs in the body. This article talks about the different ways in which smoking affects your general health and lifestyle.

How Does Smoking Affect Lung Health?

how smoking can prove detrimental for lung health?

Cigarette smoke is composed of particulate matter, toxins, and oxidative chemicals. Burning tobacco produces more than 4,000 chemicals, including nicotine, carbon monoxide, and tars. (1)

Each puff of cigarette smoke contains >1,014 oxidant molecules and >1,000 xenobiotics. (2) Exposure to cigarette smoke evokes significant biologic changes in the airway epithelium, (3) even though many smokers are phenotypically normal.

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Smoking, or exposure to secondhand smoke, (1) affects the respiratory system at microscopic levels:

  • Narrows the air passages
  • Causes chronic inflammation
  • Destroys lung tissue
  • Triggers changes leading to cancer over time (4)(5)

Cigarette smoking is also associated with an increased risk of several types of infection, (6) including tuberculosis, pneumococcal pneumonia, meningococcal disease, influenza, and the common cold.

In asthmatics, tobacco smoke can trigger an episode. (7) Also, smokers are 12–13 times more likely to die from COPD than non-smokers. (8) However, quitting smoking has an immediate benefit to the lungs. (9)

Effects of Smoking on the Different Parts of the Lungs

The chemicals present in cigarette smoke pose changes in different parts of the organ of breathing.

1. Cilia

One of the consequences of smoking is the associated reduction in mucociliary clearance. (10)

Mucociliary clearance is a vital defense mechanism against inhaled pathogens and particulates. It works by cleansing the airway surface through the coordinated action of the cilia.

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Smoking may cause damage to the cilia, reduce cilia beat frequency, and also affect cilia length, all of which result in reduced mucociliary clearance. (10)

A reduction in mucociliary clearance contributes to the increased susceptibility to respiratory tract infection, chronic obstructive lung disease, and bronchogenic carcinoma. (11)

2. Mucus-producing cells

smoking can prove harmful for mucus-producing cells

Mucus is composed of water, ions, lipids, proteins, and complex macromolecular glycoproteins called mucins, which render viscoelastic and gel-forming properties to mucus.

Airway mucus plays an important role in host defense mechanisms as a physicochemical barrier to inhaled particles and gases, bacteria, and viruses.

However, the overproduction of mucus is harmful, which is a distinguishing feature of chronic inflammatory airway diseases. (12)

Cigarette smoking is the leading cause of COPD. Oxidative stress plays a key role in smoking-induced abnormal airway mucus production, which can lead to the formation of mucus plugs. (13) Smoking also causes goblet cell hyperplasia. (14)

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3. Airways

Cigarette smoke contributes to or exacerbates airway diseases, such as asthma and COPD, where airway hyperresponsiveness and airway smooth muscle proliferation are key features.

While factors such as inflammation contribute to asthma, airway smooth muscle proliferation is one of the key pathological changes in asthma. (15)

The mechanisms by which cigarette smoke affects airway smooth muscle are still being investigated. (16) However, oxygen radicals generated as a result of cigarette smoke exposure might be causative of increased lung cell proliferation.

Chronic tobacco smoking leads to a definite tendency to narrowing of both the large and the small airways.

4. Alveoli

Emphysema, characterized by the enlargement of alveolar spaces, together with the destruction of alveolar walls, is classically believed to develop when mediators of tissue injury exceed the protective mechanisms within the lung. (17)

A variety of repair functions are affected by toxins present in cigarette smoke. Cigarette smoke can impair the repair functions of fibroblasts, epithelial cells, and mesenchymal cells.

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Far and away, the most common cause of pulmonary emphysema is cigarette smoking. (18) Cigarette smoke causes an inflammatory response in the lower respiratory tract that can damage lung structures.

Volatile components of cigarette smoke can also inhibit the function of mesenchymal cells. (17) Thus, cigarette smoking not only damages the lungs but also inhibits repair of the lungs.

5. Epithelial and endothelial cells

smoking can prove toxic for epithelial and endothelial cells

The epithelial and endothelial cells in the lungs participate in repair responses. Cigarette smoke is toxic to both endothelial cells and their circulating precursors. Smokers have reduced circulating vascular endothelial cell precursors. (19)

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Smoke-mediated endothelial damage or impairment of endothelial cell maintenance could lead to emphysema, as the death of endothelial cells can cause emphysema. Similarly, smoke inhibits airway epithelial cell chemotaxis and proliferation.

Final Word

Smoking is the number one cause of COPD deaths and lung cancer. Exposure to cigarette smoke has various detrimental effects on the lungs, ranging from reduced mucociliary clearance to altered DNA modification. Therefore, to prevent such complications, it is best to quit smoking altogether.

Continue Reading Continue ReadingBest Exercises That Increase Lung Capacity
References
  1. Naeem Z. Second-hand smoke – ignored implications. International journal of health sciences. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4538886/. Published April 2015.
  2. KanchanMohod. Circulating Lipid Peroxide and Antioxidant Status in Cigarette Smokers: An Oxidative Damage Phenomena. https://www.researchgate.net/publication/262726133. Published 2014.
  3. Lee J, Taneja V, Vassallo R. Cigarette smoking and inflammation: cellular and molecular mechanisms. Journal of dental research. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3261116/. Published February 2012.
  4. Furrukh M. Tobacco Smoking and Lung Cancer: Perception-changing facts. Sultan Qaboos University medical journal. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749017/. Published August 2013.
  5. Moktar A, Ravoori S, Vadhanam MV, Gairola CG, Gupta RC. Cigarette smoke-induced DNA damage and repair detected by the comet assay in HPV-transformed cervical cells. International journal of oncology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896024/. Published December 2009.
  6. Jiang C, Chen Q, Xie M. Smoking increases the risk of infectious diseases: A narrative review. Tobacco induced diseases. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7398598/. Published July 14, 2020.
  7. Quirt J, Hildebrand KJ, Mazza J, Noya F, Kim H. Asthma. Allergy, asthma, and clinical immunology: official journal of the Canadian Society of Allergy and Clinical Immunology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6157154/. Published September 12, 2018.
  8. Health Effects of Cigarette Smoking. Centers for Disease Control and Prevention. https://www.cdc.gov/tobacco/data_statistics/fact_sheets/health_effects/effects_cig_smoking/index.htm. Published April 28, 2020.
  9. Wu J, Sin DD. Improved patient outcome with smoking cessation: when is it too late? International journal of chronic obstructive pulmonary disease. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3144846/. Published 2011.
  10. Leopold PL, O’Mahony MJ, Lian XJ, Tilley AE, Harvey B-G, Crystal RG. Smoking is associated with shortened airway cilia. PloS one. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2790614/. Published December 16, 2009.
  11. Tilley AE, Walters MS, Shaykhiev R, Crystal RG. Cilia dysfunction in lung disease. Annual review of physiology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465242/. Published 2015.
  12. Shen Y, Huang S, Kang J, et al. Management of airway mucus hypersecretion in chronic airway inflammatory disease: Chinese expert consensus (English edition). International journal of chronic obstructive pulmonary disease. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5796802/. Published January 30, 2018.
  13. Antus B. Oxidative Stress Markers in Sputum. Oxidative medicine and cellular longevity. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4738959/. Published 2016.
  14. Kim V, Oros M, Durra H, et al. Chronic bronchitis and current smoking are associated with more goblet cells in moderate to severe COPD and smokers without airflow obstruction. PloS one. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315442/. Published February 3, 2015.
  15. Doeing DC, Solway J. Airway smooth muscle in the pathophysiology and treatment of asthma. Journal of applied physiology (Bethesda, Md.: 1985). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3633438/. Published April 2013.
  16. Wylam ME, Sathish V, VanOosten SK, et al. Mechanisms of Cigarette Smoke Effects on Human Airway Smooth Muscle. PloS one. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4468194/. Published June 15, 2015.
  17. Rennard SI, Togo S, Holz O. Cigarette smoke inhibits alveolar repair: a mechanism for the development of emphysema. Proceedings of the American Thoracic Society. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2647656/. Published November 2006.
  18. Smoking and COPD. Centers for Disease Control and Prevention. https://www.cdc.gov/tobacco/campaign/tips/diseases/copd.html. Published March 23, 2020.
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