As per the CDC, in 2018, an estimated 16 million people in the United States live with a smoking-related disease, and 1 out of 5 deaths is due to cigarette smoking. Smoking-related maladies can vary from cancer, heart disease, stroke, diabetes, osteoporosis, and lung diseases like chronic obstructive pulmonary disease (COPD). While cancer-related deaths are the leading cause of premature deaths, respiratory diseases like COPD rank second among heavy smokers. An estimated 328 million people have COPD worldwide. COPD was also estimated to be the seventh and tenth leading cause of disability in high-income countries and low or middle-income countries, respectively. COPD is a clinical manifestation associated with the lung, leading to shortness of breath, cough, exercise intolerance, and sputum production. Lung function tests and chest X-ray primarily detect COPD. Although constant exposure to pollutants and particulate matter can lead to progressive COPD, a survey conducted by Copenhagen City Heart study for a period of 25 years showed that the absolute risk of developing COPD among smokers is 25% higher than non-smokers. Another survey conducted in South Carolina similarly reported that 25.6 % of active smokers who had smoked ≥ 30 years had developed COPD.
Effects of cigarette smoke on the lungs
The human lung is a complex system involved in gas transfer. It possesses a large surface area (nearly 100 sq meters), which begins at the trachea, gradually branching out as bronchioles (airways) to over millions of closed air sacs, termed alveoli, where gas transfer takes place. An average human inhales about 10,000 liters of air per day. The lung possesses an elegant set of defense mechanisms (cilia, mucus, and immune cells like neutrophils, alveolar macrophages, and dendritic cells) to protect itself from inhaled particulate material and pathogens. Cigarette smoking leads to particulate material deposition in the lung. Inhaled tobacco smoke moves from the mouth through the upper airway, ultimately reaching the alveoli. As the smoke moves more deeply into the respiratory tract, more soluble gases are adsorbed, and particles are deposited in the airways and alveoli.
Cigarette smoking causes severe pathophysiological changes in the lung, including mucus production, airways remodeling, tissue damage, and accelerated decline in lung function. Constant exposure of cigarette smoke initiates a cascade of chronic inflammation characterized by activation and infiltration of inflammatory cells like neutrophils, T cells, and B cells into the lung.
Smoking = accelerated aging
Aging is a natural process that results in a decline in organ function and an increased vulnerability to infection and chronic diseases. The human lung none-the-less faces the same fate. Lung aging is associated with several anatomic (enlargement of alveoli without alveolar wall destruction, the reduced surface area for gas exchange, often referred to as "senile emphysema") and functional changes (reduced elastic recoil and increased gas trapping). These changes result in a progressive decrease in expiratory flow rates with age in otherwise healthy people.
Smoking induces a profound remodeling of the aged lung. As per CDC reports, approximately 80% of the COPD related deaths have been associated with smoking, and approximately 8.4 % of the US population above 65 years smoke regularly. The World health organization (WHO) states that by 2050 approximately 22% of the world population will be over 60 years of age compared to 11% in 2000.
A study in a mouse model demonstrated that cigarette smoke exposure in aged mice (12-month-old) accelerated inflammation (higher accumulation of neutrophils, macrophages, and lymphocytes in the lung) and COPD symptoms as compared to young mice (2-month-old). Cigarette smoke exposure increases collagen deposition around the airways of aged mice, enhancing stiffness resulting in difficulty in breathing. Accelerated aging was also observed in mice exposed to cigarette smoke. In short, cigarette smoke exposure elevates lung inflammation in old mice, induces changes in the immune cells, and accelerates COPD's pathophysiological hallmarks. The duration of smoking is also directly related to COPD severity. The combined effect of age and smoking duration correlates with higher lung deterioration among aged subjects (60 years and above) with over 20 years of smoking than those of the same age with only five years of smoking.
Although not completely curable, COPD progression can be eased with proper medications, like inhalers, steroids, or surgery. Inhalers are prescribed depending upon the severity of the disease and can be short-acting (inhaled just before any physical activity) like albuterol, levalbuterol, or long-acting (inhaled daily) aclidinium, arformoterol, formoterol, tiotropium, etc. These inhalers act as a quick relief and function by relaxing the muscles' stiffness around the airways. Steroids (inhalational/ oral) are prescribed to patients with worsened COPD conditions. They function by preventing airway inflammation, relaxing the airways, and preventing exacerbations. A few names of steroids are fluticasone, budesonide, roflumilast, and theophylline. Often, these steroids are given in combination with inhalers. However, prolonged use of these steroids can lead to side-effects like weight gain, osteoporosis, diabetes, and cataracts. Surgery is the option for patients who are not relieved by medication. However, they carry significant risks, such as organ rejection, and one may need to take lifelong immune-suppressing medications. Finally, COPD is a disease manifestation. Its progression can be paused with proper medication and care, like breathing exercises, avoiding pollution and smoke, a healthy lifestyle, and regular consultation with your healthcare provider.