- Smoker's lung introduction
- What is the structure of the normal lung?
- What processes determine normal function of the lung?
- What are the abnormalities (diseases) in smoker's lung?
- What happens to the lung in emphysema?
- How does emphysema come about?
- Why does smoker's lung look black?
- What happens to the airways in chronic bronchitis?
- Are smokers with COPD predisposed to developing pneumonia?
- What about lung cancer in smokers?
- Are any of the pulmonary consequences of smoking reversible?
- From what do smokers die?
Smoker's lung introduction
Cigarette smoking is associated with a wide variety of abnormalities throughout the body that cause not only illness, but also, all too often, death. Indeed, if all deaths from diseases related to smoking (lung disease, heart disease, and cancers of many different organs) were considered, a case could be made for cigarette smoking as the leading cause of death in industrialized countries. Ironically, it is also the most preventable cause of death in our society!
This photo essay will focus on smoker's lung. The term "smoker's lung" refers to the structural and functional abnormalities (diseases) in the lung caused by cigarette smoking. First, the normal structure and function of the lung will be described and illustrated. Then, the structural and functional abnormalities caused by smoking will be described and illustrated.
What is the structure of the normal lung?
We have a right lung and a left lung that reside in the chest cavity and surround the heart. A thin membrane called the pleura covers the outer surface of the lung. The air we breathe gets into the lung through an airway (path for air). Figure 1 is a diagram showing the main parts of the airway and lung.
The airway consists of the oral and nasal cavities, which connect to the voice box (larynx), which connects to the windpipe (trachea). Note in the diagram that the windpipe splits into two air passages called bronchi, one going to each lung (right and left main bronchi). The trachea and larger bronchi contain C-shaped rigid bars of cartilage in their walls. The cartilage helps to keep the airway from collapsing when there is negative pressure in the airway, as occurs when we breathe in (inhale or inspire). The right lung has three separate sections (upper, middle, and lower lobes), while the left lung has just an upper and a lower lobe. Each lobe has its own bronchi and blood supply.
Further along in the airway, within the lung, the bronchi continue to divide into ever-smaller (narrower) tubes, much like the branches of a tree. (Hence, the term tracheobronchial tree.) The walls of the bronchi contain muscles that can cause the airway to expand (widen) or contract (narrow). For example, during exercise, the airway expands to increase airflow (ventilation). Conversely, when exposed to polluted or very cold air, the airway contracts to protect the downstream tissues from injury. The smaller branches of the bronchial tree, called bronchioles, also contain muscle, but they lack cartilage. Notice in Figure 1 that the very smallest bronchioles (respiratory bronchioles) connect directly to tiny air sacs in the lung, called alveoli. Figure 2 shows a microscopic section of a normal bronchial wall.
In this picture, you can see that the bronchial wall contains cartilage and muscle, as described above. Also, note that different types of cells make up the lining (epithelium) of the bronchi (as well as of the trachea and bronchioles). One type of cell is called a goblet cell because of its shape. The goblet cells produce mucus, which lubricates the airways and traps inhaled foreign material (e.g., bacteria, viruses, and pollutants). Other cells in the epithelium are called ciliated cells, which are discussed in the next paragraph. Beneath the surface of the airway, the goblet cells and other epithelial cells are clustered into structures called bronchial glands. These glands secrete additional mucus and other lubricating fluids.
Inflammatory cells are also in the normal bronchial wall. Look again at Figure 2 and observe that they are scattered beneath the lining of the airway. These inflammatory cells, also known as white blood cells, include neutrophils, lymphocytes, and macrophages. Their job (in this situation) is to destroy and/or engulf any inhaled foreign material that becomes trapped in the mucus. In doing so, however, inflammatory cells create debris. To help dispose of the debris, most of the cells that line the airway have hair-like processes called cilia. These ciliated cells sweep and push the foreign material and debris up into the larger airways where they can be coughed up or spit out.
The lung resembles a sponge and is composed of millions of alveoli. This structure provides a huge surface for gas exchange that has been estimated to be equal to the size of a tennis court. (These tiny air sacs can be seen with a magnifying glass.) Figure 3 is a microscopic section of a normal lung, showing the alveoli.
The wall (alveolar septum) of each alveolus contains a very small blood vessel called a capillary. Blood flows slowly through each capillary to allow time for the lung to perform its main function, which is the exchange of gas (oxygen and carbon dioxide). The actual site for gas exchange is pictured in the high magnification section on the right side of figure 3. Thus, the capillary blood picks up oxygen (O2) from the inhaled air in the alveoli. At the same time, the capillary blood releases the body's waste gases, most importantly carbon dioxide (CO2), into the alveoli. (Waste gases are by-products of the body's metabolism.)
What processes determine normal function of the lung?
As just indicated, the main function of the lung is the exchange of the gases oxygen and carbon dioxide. So, the blood in the alveolar capillaries takes oxygen from inhaled air that is in the alveoli. Then, the oxygenated blood circulates through the body to deliver the oxygen to the tissues. In the exchange of gases, the blood in the alveolar capillaries releases carbon dioxide to the alveoli. Then, when we breathe out (exhale or expire), the carbon dioxide is removed from the alveoli through the airway and eliminated from body. Accordingly, three processes determine normal lung function:
- Blood supply
Ventilation is the moving of air into and out of the lung. This process requires an open (unobstructed) airway. Increasing and decreasing the size of the chest cavity is what accomplishes the movement of air. You see, as the chest cavity enlarges, a vacuum is created in the airway and air rushes in. Then, with breathing out, the chest cavity becomes smaller and air is pushed out. The muscles in the chest wall (intercostal muscles between the ribs), and the muscles in the diaphragm work together to change the size of the chest cavity. (The diaphragm is a flat muscular membrane that separates the chest from the abdomen.) In addition, when we breathe really hard, we even use muscles in the neck (referred to as accessory muscles for breathing) to help expand the chest.
Diffusion is the process that accomplishes the actual gas exchange across the alveolar walls. This process requires normal alveolar septae (the walls of the air sacs) that contain intact capillaries. Finally, a normal blood supply depends on normal capillaries, normal red blood cell counts (no anemia), and normal pumping of blood by the heart. Any disease that interferes with ventilation, diffusion, or blood supply to the lung will impair lung (pulmonary) function and decrease delivery of oxygen to the tissues of the body.
What are the abnormalities (diseases) in smoker's lung?
The major abnormalities in smoker's lung are grouped under the label of chronic obstructive pulmonary disease (COPD). It is estimated that 40 million people worldwide suffer from COPD. COPD is the 4th leading cause of death in the USA. Even more disturbing is the fact that COPD is the only one of the "top 5" causes of death to increase in the past decade. While COPD has been thought of as a disease of men, it is estimated that by the year 2010 there will be more women than men affected by COPD. These statistics are especially sad because COPD is a preventable disease by stopping smoking; unfortunately, this is easier said than done. About 70% of smokers want to quit, but only 7% who try are smoke free after one year. However, one should not give up. Numerous tries, sometimes more than 10, and professional help often are needed, but the health benefits of smoking cessation make it worth the effort.
COPD is made up of two major, related diseases. One, emphysema, involves the lung alveoli, and the other, chronic bronchitis, involves the bronchial airway. (Both conditions are discussed below.) In this essay, I will use the term chronic bronchitis to include chronic bronchiolitis and chronic respiratory bronchiolitis. I do this because these three conditions have the same pathology (structural abnormalities), cause the same symptoms, and differ only in their location in the airway. At any rate, some smokers primarily have emphysema and some primarily have chronic bronchitis. Most, however, have a combination of these two diseases.
What happens to the lung in emphysema?
In emphysema, the walls of the air sacs (alveolar septae) are destroyed. Consequently, the individual air spaces (alveoli) become larger but irregular and decreased in number. These larger spaces are less efficient than normal sized alveoli for gas exchange. Thus, emphysema impairs diffusion of oxygen and carbon dioxide (gas exchange). The more extensive the emphysema, the poorer the gas exchange becomes. Also, in emphysema, the capillaries are destroyed with the rest of the alveolar wall. As a result, emphysema also disrupts the normal blood supply. Figure 4 contrasts the nasty appearance of a smoker's emphysematous lung with a normal lung.
Emphysema usually starts in the upper lobes of the lung and, as depicted in this photo, is more severe in the upper lobes for complex reasons. That is, the abnormal (enlarged and irregular) air sacs (alveoli) are more prominent in the upper lobes. (The blood vessels in the lungs should not be mistaken for the abnormal air sacs.)
In someone with severe emphysema, the entire chest actually can enlarge. What probably happens is that the patient's extra (compensatory) efforts to suck in as much air as possible (to increase ventilation) contribute to enlarging the lungs and the chest. Thus, a person with severe emphysema often develops what has been described as a barrel-chest.
How does emphysema come about?
Simply put, the cigarette smoke attracts inflammatory cells (white blood cells, including neutrophils, lymphocytes, and macrophages) into the lung. Then, the inflammatory cells release substances called proteases. The proteases dissolve the proteins in the alveolar walls (septae) and thereby destroy the septae. As a result, the alveoli join together (coalesce) to form the larger, irregular, inefficient air sacs.
It turns out that about half of all smokers develop emphysema. Mild emphysema is seen occasionally in non-smokers and may be due to passive smoking (exposure to other people smoking, or "secondhand smoke") and industrial air pollution. Severe emphysema, however, is seen only in smokers or in some people with rare inherited diseases (e.g., alpha-1-antitrypsin deficiency). Still, it takes about 30 years of smoking to develop fatal emphysema. This is because people usually don't die from emphysema until more than 60% of the lung tissue is affected.
Why does smoker's lung look black?
The lung is connected and exposed by the airways to a potentially noxious outside world. Accordingly, the alveolar spaces normally contain specialized scavenger cells, called alveolar macrophages. The job of these macrophages is to engulf (phagocytize) any possibly harmful foreign material that enters the lung through the airways.
As you can imagine, cigarette smoke contains many impurities that are inhaled in great numbers directly into the lung. For this reason, the alveolar spaces of the smoker contain numerous scavenger cells (macrophages) that are filled with engulfed (phagocytized) particles of impurities and debris, as illustrated in
Under the microscope, with this high magnification, you can actually see the black and brown engulfed particles in the alveolar scavenger cells. Indeed, smoker's lung may have so much of this particulate material that the lung looks gray-black to the naked eye. Most of the time, you don't need a microscope to tell if someone is or was a heavy smoker. A naked eye examination of a smoker's lung will usually reveal an enlarged gray-black lung with enlarged air spaces (the emphysema, as you saw in Figure 4 and will see again in Figure 8).
What happens to the airways in chronic bronchitis?
In chronic bronchitis, smoke damages the cells that line the airway (epithelial cells). Nicotine is one of the many components of cigarette smoke that is directly toxic to the lining cells of the airway. (Of course, the nicotine is also addictive.) The tissue damage attracts inflammatory cells. These cells then release enzymes that further damage the lining cells of the airway and stimulate goblet cells to increase in number and to increase mucus production. Figure 6 is a microscopic section of a bronchial wall in a smoker with chronic bronchitis.
The major consequence of chronic bronchitis is airway obstruction. In fact, this figure demonstrates mucus and debris blocking the bronchial airway. Indeed, the most important cause of airway obstruction in chronic bronchitis is blockage by mucus, inflammation, progressive scarring (fibrosis), and/or narrowing (constriction) of the airways. As a result of the bronchial blockage, gases cannot get to and from the alveoli. In other words, chronic bronchitis interferes with ventilation.
It is important to know that people with asthma likewise have chronic bronchitis with airway obstruction. In asthma, however, the cause of obstruction is somewhat different and the obstruction usually occurs in attacks that are reversible. In any case, both smokers and asthmatics with bronchitis may cough, wheeze, and spit up thick mucus (sputum) from the lung.
Are smokers with COPD predisposed to developing pneumonia?
The answer is yes. As previously mentioned, smoking increases mucus production and impairs the clearing action of the cilia in the airway. Also, the addition of bacteria, inflammatory cells, and damaged lung cells to the secretions in the airway and lung make the secretions especially thick, tenacious, and difficult to clear. Therefore, in such a stagnant and nutritious (the mucus) environment, bacteria can flourish and cause infection of the lung (pneumonia). Furthermore, even the inflammatory cells are damaged by tobacco smoke so that their ability to fight infection is diminished.
For all of these reasons, pneumonia is not only more common, but it is often also more severe in smokers with COPD (chronic obstructive pulmonary disease, that is, emphysema and/or chronic bronchitis) than in non-smokers without COPD. Moreover, the inflammatory cells that accumulate in the lung to fight off the infection can fill the alveolar spaces and thereby further limit diffusion of oxygen and carbon dioxide. Therefore, smokers with COPD, who already have impaired breathing (pulmonary function), often become much worse when there is a superimposed infection of the lung (pneumonia). Figure 7 is a microscopic section of a lung with pneumonia in a patient with COPD.
Notice that most of the alveoli are filled with inflammatory cells. Some alveoli, however, are unaffected and empty because the involvement of this lung with pneumonia is patchy.
What about lung cancer in smokers?
Smoke contains more than 60 carcinogens (chemicals that cause cancer) and about 200 known toxic substances. Scientists are still learning about how carcinogens work and why only some people who smoke get lung cancer. Genes are the hereditary units in chromosomes and appear to have a lot to do with a person's susceptibility to cancer. The genes are made up of DNA (deoxyribose nucleic acid), which controls how cells divide and reproduce (proliferate). Damage to DNA from cigarette smoke can lead to uncontrolled cell proliferation and growth, which is what cancer is finally all about.
It is of interest that some smokers develop COPD, some develop lung cancer, some get neither, and some get both. We really don't know the reason for these different susceptibilities. Besides that, lung cancer from smoking can take a number of different forms. For example, the cancer cells can resemble cells of the skin (squamous cell carcinoma), cells of the bronchial glands (adenocarcinoma), or specialized cells of the nervous system (neuroendocrine carcinoma). Figure 8 shows an adenocarcinoma in a smoker's lung with severe emphysema.
What do you think the outcome (prognosis) is for this patient with lung cancer? Well, almost all types of lung cancer are particularly deadly. Thus, if a lung cancer is more than an inch or so in diameter (as in this patient) or has spread outside of the lung, fewer than 50% of affected individuals will survive another 5 years. And that is even with the best of therapy. What's more, consider a cancer that is less than an inch in size (or not large enough to be seen on a chest X-ray) and is confined to the lung. Unfortunately, even if such a cancer is completely removed by surgery, about 25% of individuals will still die from the cancer in less than 5 years from the time of diagnosis. The reason for this poor outcome (prognosis) is that lung cancers tend to spread (metastasize) early in the course of disease to other organs, most often the brain, liver, and bone.
Are any of the pulmonary consequences of smoking reversible?
First, the bad news is that emphysema is not reversible. But now, the good news! If a person stops smoking, the inflammatory changes (chronic bronchitis) in the airways probably will go away. Furthermore, when a person stops smoking, the risk of developing lung cancer decreases, although it never goes back to normal. In other words, the risk of cancer in ex-smokers is less than in smokers, but remains greater than in non-smokers.
From what do smokers die?
Remarkably, despite a wealth of information on death rates (mortality) from cigarette smoking, little information is available on the specific causes of death in smokers. Smokers with COPD can die from lack of oxygen (hypoxia) in the tissues of the body. The hypoxia occurs because there is so little functioning lung left and/or the effort of breathing is so great that affected individuals just stop breathing from exhaustion. Other important causes of death in smokers include lung infection (pneumonia), lung cancer, cancers of the digestive, urinary, and genital systems, and leukemia. Indeed, because smoking can cause cancer in so many organs, 30% of all cancer deaths can be related to cigarette smoking.
Nevertheless, because smoking is such a powerful risk factor for the development of coronary atherosclerosis (hardening and blockage of the arteries of the heart), heart disease is by far the most common cause of death in smokers. Moreover, since autopsies are done in less than 10% of patients who die in hospitals and less than 1% of patients who die in nursing homes, we really can't prove why most smokers die. You see, even though a clinician is often correct about the cause of a person's death, only an autopsy can be definitive.
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Medically reviewed by James E. Gerace, MD; American Board of Internal Medicine with subspecialty in Pulmonary Disease
"Cigarette smoking and other risk factors for lung cancer"