From the Guidelines
Smoking leads to significant and irreversible changes in the lungs, primarily through chronic inflammatory responses, oxidative stress, and damage to the airways and alveoli, resulting in conditions such as emphysema, chronic bronchitis, and increased risk of lung cancer. The mechanisms by which smoking causes these changes are multifaceted, involving the introduction of thousands of harmful chemicals into the respiratory system, including nicotine, tar, carbon monoxide, and various carcinogens 1. These toxins irritate the airways, causing inflammation and increased mucus production, and over time, destroy the tiny hair-like structures called cilia that help clear mucus and debris from the lungs, leading to chronic cough and increased risk of infections.
The smoke also damages the alveoli, the tiny air sacs responsible for oxygen exchange, causing them to lose elasticity and eventually break down, resulting in emphysema. Additionally, smoking narrows the airways through inflammation and excess mucus, contributing to chronic bronchitis. The carcinogens in tobacco smoke can cause genetic mutations in lung cells, potentially leading to lung cancer. These changes occur progressively with continued smoking, but quitting can slow or stop this damage, allowing the lungs to begin healing 1.
Key points to consider include:
- The chronic inflammatory response and oxidative stress caused by smoking lead to the abnormalities characteristic of COPD 1.
- The disease continues to progress in a substantial proportion of patients, even after inhalation of the offending agent ceases, suggesting other pathobiological processes are at play 1.
- Smoking cessation is essential at all stages of the disease and can prevent the accelerated decline seen in many patients with COPD 1.
- Participation in an active smoking cessation programme leads to a higher sustained quit rate, especially when nicotine replacement therapy is included 1.
Given the evidence, the most effective way to prevent or slow the changes in the lungs caused by smoking is to quit smoking, as this can prevent the accelerated decline in lung function and reduce the risk of developing serious conditions like COPD and lung cancer 1.
From the Research
Changes in the Lungs due to Smoking
- Smoking leads to various changes in the lungs, including inflammation, epithelial damage, and remodeling of the airways 2
- The lung is particularly susceptible to oxidative stress caused by chronic exposure to cigarette smoke, leading to respiratory diseases such as chronic obstructive pulmonary disease (COPD), pulmonary fibrosis (PF), and lung cancer 3
- Cigarette smoke contains over 4,500 components, including carbon monoxide, nicotine, oxidants, fine particulate matter, and aldehydes, which are considered the principal factors driving the pathogenesis and progression of pulmonary disease 4
Mechanisms of Lung Damage
- The infiltration of inflammatory cells to mucosa, submucosa, and glandular tissue caused by inhaled cigarette smoke is responsible for the destruction of matrix, blood supply shortage, and epithelial cell death 4
- Oxidative stress caused by chronic exposure to cigarette smoke can lead to inflammation, apoptosis, and senescence in the lungs 3
- Soluble epoxide hydrolase (sEH) is involved in the metabolism of endogenous chemical mediators that play an important role in inflammation, and inhibition of sEH can attenuate tobacco smoke-induced inflammation 2
Lung Diseases Associated with Smoking
- COPD and lung cancer are major lung diseases affecting millions of individuals worldwide, and are closely related to smoking 4
- Cigarette smoking is considered a principal aetiological factor responsible for the development of certain diffuse interstitial and bronchiolar lung diseases, including respiratory bronchiolitis-interstitial lung disease (RB-ILD), desquamative interstitial pneumonia (DIP), and adult pulmonary Langerhans' cell histiocytosis (PLCH) 5
- Emphysematous destruction of the gas exchanging tissue and thickening of the walls of the small conducting airways contribute to airflow limitation in COPD 6