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Cigarette Smoking |
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The lungs are the target organs for much of the damage associated with cigarette smoking. The lungs are absolutely essential for life, but also are very vulnerable to the outside world. With every breath, environmental air comes into intimate contact with the delicate structures of the lower respiratory tract. The air we breathe undergoes some preliminary processing before it reaches the lungs, however. It is filtered to remove larger particles, humidified and then warmed to body temperatures. Approximately 10,000 liters of air pass through the nose every 24 hours requiring about three quarters of a quart of water to properly humidity every day. These defense mechanisms are efficient means to remove most of the noxious environmental pulmonary irritants inspired prior to reaching the lung surface. However, these defenses can be easily overwhelmed by excessive exposure such as with smoking a cigarette. While the upper respiratory tract is excellent at removing particulate
matter, it is very inadequate in removing gaseous contaminants such as
carbon monoxide, phosgene and chlorine gases. Some of these toxic
gases are partially removed as they dissolve in secretions from the mucous
membranes lining the upper respiratory tract. However, much of these
gases successfully reach the lower respiratory tract and can then produce
severe damage not only to the lungs, but also to the rest of the body.
Some of the poisonous gases inhaled with each cigarette puff include carbon
monoxide, carbon disulfide, hydrogen cyanide, and nitrogen dioxide.
The fundamentals of pulmonary anatomy must be first understood in order to appreciate what smoking can do to the lungs, how it does it and how the damage can be treated. The normal lung must first be understood before the abnormal can be studied. Now, I do not intend to delve too deeply into pulmonary anatomy for several reasons, not the least of which is that the reader is probably not too interested. Much pulmonary anatomy just is not necessary to learn when studying the effects of smoking. Also, I don't want the reader just to simply skip this section and go onto what is hoped to be more interesting sections because this section is very important as it lays the foundation for future discussion. With that in mind, let's discuss the pertinent fundamentals of pulmonary anatomy. When you take a breath of air, what you are really trying to do is to take in life sustaining oxygen, and to get rid of carbon dioxide, a waste product. In order to do this, the oxygen must get down to the lungs from the outside air, and likewise carbon dioxide (a waste produce produced by the body) must get from the lungs to the outside. Air must first be inhaled through the nose, down the throat, past the vocal cords (larynx), into the windpipe (trachea) down the smaller windpipes (bronchi) and into the alveoli where the real action occurs. Inspiration is under voluntary control but usually is a reflex action initiated by certain parts of the brain. There are many stimulation to respiration, but one of the most powerful is carbon dioxide. When this chemical (a waste produce by metabolism) gets too high, it stimulates the respiration centers to begin a breath. The major muscle of respiration, the diaphragm, then contracts from the neural input sent out by the brain, producing a negative pressure within the chest cavity. This negative pressure then draws air into the chest where gas exchange (oxygen for carbon dioxide) can then occur. The nose, besides serving as decoration for the face, serves several important functions. The nose helps to warm and humidify the inspired air so that the delicate mucus membranes of the lower lung won't be dried out. There are hairs in the nose which filter out larger particles so they won't pass into the lungs. The throat has organized lymph nodes (such as the tonsils) which survey and kill unfriendly bacteria before they have a chance to cause an infection. The trachea is a hollow tube that is partially surrounded by cartilage, and transports the air down to the lungs themselves. The trachea can deform itself allowing for an effective cough. The trachea can be a site of cancer, but lung cancer much more frequently occurs further down in the lungs. Once past the trachea, the oxygen then has to travel into either the right or left lung through either the right or left mainstem bronchus. A bronchus is basically a hollow tube just like the trachea but where the cartilage is not as well organized. The bronchi also produce mucus which helps keep the lungs moist and clean, have lymph nodes, produces antibodies to kill bacteria. Once into the mainstem bronchus, the oxygen passes through successively smaller and smaller branches until it finally gets to the bronchioles, which are simply smaller bronchi that are not invested with cartilage. After several more divisions, the oxygen now passes into the terminal bronchioles, respiratory bronchioles, alveolar ducts, alveolar sacs, and finally into the alveoli themselves which is where the action occurs. Cigarette smoking can affect the lungs anywhere along this long pathway from the mouth to the alveolus. Cigarette smoke may adversely affects the lungs either through lung cancer (which we will have discuss in some detail later on) and in chronic obstructive pulmonary disease, or COPD. COPD is divided into two main categories; that which mainly affects the bronchi (or chronic bronchitis), and that which mainly affects the alveoli (or emphysema). The alveoli are incredible structures approximately .01 inch in diameter. Each alveolus is surrounded by a network of fine vessels or capillaries. It is the interaction between the alveolus and its surrounding capillaries which allows for an exchange of oxygen for carbon dioxide to occur. The blood that comes to the lungs from the heart is high in carbon dioxide but low in oxygen. This blood has to enriched with oxygen and depleted of its load of carbon dioxide before it can be sent out to the rest of the body. This transfer occurs at the level of the alveolus when oxygen moves by diffusion from the alveolus into the capillary net and picked up by the hemoglobin within red blood cells, and carbon dioxide is transferred from the surrounding capillaries and into the alveoli to be expelled. This transfer of gases has to occur all the time, 24 hours a day or the patient will simply die from too little oxygen and too much carbon dioxide. Obviously, damage which occurs to this delicate capillary-alveolar structure will make this gas transfer more difficult and this is exactly what happens in emphysema. This damage, when sufficiently severe, causes severe shortness of breath with the least little exertion due to an inability of their destroyed lungs to assimilate oxygen or discharge carbon dioxide. As these people exercise, oxygen levels in their blood will fall producing a severe strain upon their heart and other muscles. Carbon dioxide levels may rise making these patients severely uncomfortable and short of breath. The lungs damage may become so severe that the lung structure becomes totally destroyed in several areas leaving large holes, called bullae. These bullae have no gas exchange ability whatsoever, and merely serve to waste ventilatory effort as air still goes in and out of them but no gas exchange occurs. Unfortunately, they frequently become infected which may require hospitalization for intravenous antibiotic treatment. Additionally, they are prone to burst open producing a pneumothorax or collapsed lung. A collapsed lung can be particularly dangerous in patients who are already significantly short of breath. Patients with emphysema generally maintain adequate oxygen levels in their blood (until the very end) although they must work very hard to do so. This extra work of breathing can exert a heavy toll on these subjects leaving them emaciated and unable to fight any trivial infection. Because emphysema is associated with a permanent destruction of these structures which will not simply grow back, there is really very little that the pulmonary physician can do to make the patient feel significantly better. Most of the drugs that are given to patients with emphysema are bronchodilators. However, the bronchi are relatively spared in patients with severe emphysema and these agents rarely have any significant effect. These patients are frequently placed on bronchodilator drugs and oxygen as their disease progresses because there is unfortunately rather little else to do. It has not yet become possible for medical science to grow new lungs, especially in people who continue to smoke! The other type of COPD is called "chronic bronchitis", and is different from emphysema in that it effects primarily the bronchi, or the breathing tubes, while sparing the alveoli. Cigarette smoke is very irritating to these breathing tubes, as you might imagine. Just remember when you started smoking just how irritating to your throat and lungs the smoke was, and how it made you cough. The constant irritation causes constant inflammation, which results in several pathologic changes in the airways. Mucus glands are ordinarily very important for they keep the lungs moist and the mucus they produce serves as a line of defense against bacteria. The mucus in the lungs is in constant motion, moving inhaled particles, bacteria, or other contaminants toward the throat where they can be swallowed or expectorated. Mucus ordinarily forms a thin coating along the airways and its presence is ordinarily not even noticed by a healthy individual. Such is not the case, however, in these subjects stricken with chronic bronchitis, for they have abnormal mucus production due to the incessant irritation of their airways with smoke. This abnormal production is more than just a nuisance to these patients, however, for not only is there too much mucus, but it is also of an increased viscosity and much thicker than normal. Now, as if this were not bad enough, this thickened abnormal mucus gets infected much more easily than the thin layer that is normally present. When this mucus gets infected, it gets thicker still. This thick, infected mucus produces an obstruction in the bronchus, making it much more difficult for the patient with bronchitis to breath. When this infection of the mucus occurs, there is usually adjacent infection of the bronchus, and an acute bronchitis occurs. This can be associated with a mild fever, a change in the color of the mucus from a grayish-white to a yellow color, and increased shortness of breath. The physician usually treats the episode of acute bronchitis with antibiotics in an attempt to kill the bacteria which are causing the infection. The trouble really begins, however, when this bronchitis extends further down into the lungs and produces an infection of the alveoli, or a pneumonia. When the alveoli are infected, they frequently get flooded with fluid that leaks out from the surrounding capillary bed. This fluid, which is swimming with the infecting bacteria, makes the alveoli unable to exchange gas with the capillary net since the alveoli no longer contain air. Then the patient really begins to complain of possibly rather severe shortness of breath, high fevers, increased sputum production, and the condition may become life threatening.. But it does not stop there. Muscle (not the type of muscle that is present in an arm muscle, but something called "smooth muscle") surrounds each bronchus. Cigarette smoke not only irritates the mucus glands in the bronchi, but it also frequently makes this muscle significantly more reactive. This means that any minor irritation may cause the muscle to contract and thereby narrow the bronchus. Now this is the last thing that the patient needs. If anything, our subject would like to have wider airways so that air could get around the voluminous thickened mucus produced by the irritated glands. Yet, precisely the reverse happens. As the airways become narrower and narrower (called "bronchospasm"), the air that passes through them has to flow quicker, air turbulence occurs, and a wheeze is produced. Frequently, this wheeze may be audible not only to the physician listening through the stethoscope, but also to the patient. It is this high pitched wheeze that may alert the patient and the doctor that something evil is happening in the airways. Once this happens, again the patient becomes markedly shorter of breath, feels tightness in the chest, and very uncomfortable. Fortunately for the patient, however, the physician can often
make the the patient with chronic bronchitis feel significantly better
with medications that relieve the bronchospasm. Even though the precise
mechanisms by which they work are different, they all will help to reduce
the amount of smooth muscle spasm, open up the airways, and allow the patient
to cough up the thickened mucus better. However, the story is not
all good. Even though these medications may make the patient feel
significantly improved, all of them are associated with possibly rather
severe side-reactions. They must be given in precise dosages, and
be closely regulated by the physician. Too much of some of these
medications may produce very severe, possibly life threatening side reactions
of their own. So, the drugs are really two edged swords, and it would
be much better if the patient did not get into trouble in the first place
by smoking.
Cigarette smoking is the most important cause of lung cancer by far. The evidence is so overwhelming that cigarette smoke causes cancer (and is just not associated with it) that any reasonable argument to the contrary is untenable. This causal relationship much be examined and contemplated before an enlightened decision can be exercised. In the final analysis, it is truly up to you (and you alone) as to whether the benefits you feel are derived from smoking are worth the potential risk of serious health injury. But before you can make that decision, get the facts. do not make any decision without having a firm grasp of the pertinent information, or you may simply come to the wrong decision. Recently, information concerning cigarettes and lung cancer has been exploding. We are beginning to understand as never before not only that cigarette smoking causes lung cancer, but also the cellular and subcellular details as to how. The average smoker, however, simply does not have ready access to this information, however. There are many excellent monographs about drug or alcohol abuse, self-help groups, religious interventions, and telethons. But in the field of cigarette cessation, the information and social outcry is simply not there. Smoke, the combustion produce of tobacco, is a complex mixture of thousands of chemical agents. Many of these substances are organic compounds which have been identified, but not yet thoroughly studies. Additionally, cigarette manufacturers have been placing new organic additives to tobacco in an attempt to change the tobacco aroma or taste. naturally, these artificial additives also form combustion products whose cancer causing potential is largely unknown. It is their complex mixture or organic molecules that the smoker's lungs are exposed to with each puff, often in concentrations far above that found in urban populations. Try this experiment. Take a clean handkerchief and go to the dirtiest part of town where the air is literally filled with all manner of filth and soot. Take a deep breath in, and exhale through the clean white handkerchief. Now, light up your favorite brand of cigarette, inhale deeply, and exhale through the same cloth. what you will see is a dark brown spot from the cigarette smoke, with no stain at all from the industrial pollution. Go out and try it if you do not believe me, but the concentration of filth inhaled with each puff of your cigarette is far greater than that produced by the worst urban industrial pollution. Cancer can be directly produced by carcinogens, or promoted by co-carcinogens. Carcinogens are agents which can produce cellular transformation leading to cancerous changes. Tobacco smoke is replete with potent carcinogens including such organic substances as benz(a)pyrene. Cocarcinogens are substances which have little or no direct carcinogenic potential but can increase the cancer causing ability of carcinogens by either increasing the number of cancers caused, or by decreasing the time required for the cancer to occur. Smoke, as might well be expected, has co-carcinogens as well as carcinogens, which increase the cancer causing ability of the carcinogens. The evidence that these substances can cause disease in humans has been firmly established after years of painful investigation. Pathologic specimens from patients who smoke but who died show extensive precancerous changes when compared to lung obtained from patients who did not smoke. Experimental animals easily develop lung cancer when they are put on smoking machines or when smoke tar extract is painted on their airways. The most damning indictment of cigarettes is the relative chance of people who smoke to develop lung cancer compared to those who do not smoke. When this is done, a definite relationship can be seen between the extent of smoking (number of cigarettes smoked per day) and the chance of getting lung cancer. The more you smoke, the greater your chances are of getting lung cancer. Also, it is important to realize that if you do stop smoking today, your chances of lung cancer do not go down to zero tomorrow. Unfortunately, a lung cancer may take many years to develop symptoms, and years to grow large enough to be visible on a chest X-ray. Also, the chronically inflammation in your airways after having smoked for so many years is a fertile ground for the development of lung cancer. Actually, it may well take 10 years or more before your risks of lung cancer approach that of the normal non-smoking population. But your risk will get less tomorrow only if you stop smoking today! Many of you are now no doubt wondering about other types of exposure you may have had, its relationship to smoking, and the development of lung cancer. The most important exposure in this regard is asbestos. If you have been exposed to asbestos in your working life, even if many years or even decades ago, then it is of the utmost and absolute urgency that you must stop smoking, this simply cannot be emphasized too much. That past exposure to asbestos and your smoking will increase your risk of lung cancer almost 100 times over the non-smoker. You can dramatically reduce that figure if only you would stop that smoking - NOW! Also, it does not matter whether you are now having asbestos exposure (which is unlikely due to the known dangers) or asbestos exposure 30 years ago. It is still there, in your lungs, ready to strike out. Asbestos is truly a remarkable substances due to its fire retardation ability, and was present just about everywhere, including many schools and office buildings. But some jobs are associated with an especially high risk of exposure, including shipbuilding, pipe-fitting, general construction, and building demolition. If you have any of these exposures or have been exposed to asbestos in another kind of work, it is simply imperative that you stop smoking, and you certainly should see a physician and get checked out. Other occupational exposures may increase your risk of lung cancer, especially when combined with smoking. These include uranium, nickel, cobalt, coke, arsenic, and mustard gas. Naturally, you certainly should not smoke if you have any of these exposures either. The effect of some other lung toxins, such as a dusty environment or air pollution is much less clear and much more controversial. Air pollution is a complex mixture of particulate matter and various gases. Sulfur dioxide, nitrogen dioxide and ferric oxide are all found as major constituents of air pollution, and all have been implicated in animal studies as being co-carcinogens when combined with the carcinogens readily found in tobacco smoke. However, their role, if any, in the production of lung cancer in humans remains unclear. There is a slight increase in lung cancer in urban residents when compared to rural residents, but it is unclear whether this may simply represent occupational differences between the two groups. Lung cancer is a very diverse disease. Some patients are caught early enough and can have their cancer cured with surgery. Others can be cured with radiation therapy and rarely with chemotherapy. However, those patients who can be cured of their disease is relatively small. Unfortunately, by the time the patient develops symptoms from lung cancer, goes to a physician and has a diagnosis made, it is frequently already too late for a cure. This is the tragedy of lung cancer - that it is largely such a preventable disease, and it is so often fatal. Out of all patients who develop lung cancer, only about one-third will be able to have surgery performed, and of these, about half will be found to have extensive disease at the time of surgery and be inoperable. And, unfortunately, many who have surgical removal of their cancer will have a recurrence of their tumor either in their remaining lung or have spread of their cancer to other organs. Clearly, the best "treatment" for lung cancer is never to get it in the first place, and the best way to do that is to never smoke. Carbon monoxide is a colorless, tasteless, odorless gas that is
formed by the incomplete combustion of tobacco (and other combustibles)
and is another major toxin produced by cigarette smoking. Carbon
monoxide is different from the other toxins we have discussed, however,
because its major toxicity is on the blood. Hemoglobin is a protein
found in red blood cells which carries oxygen from the lungs to the rest
of the body. Hemoglobin is a carrier protein with an affinity or
attraction, for oxygen. Without hemoglobin, not enough oxygen could
be carried by the blood to support life and we would all die. Carbon
monoxide has a greater affinity for hemoglobin than oxygen (about 250 times
greater affinity) and will attach itself to all available hemoglobin, rather
than letting oxygen get on board. Only a small amount of carbon monoxide
can displace large quantities of oxygen from hemoglobin because of its
much greater affinity, thereby starving you from oxygen.
In addition to the effect carbon monoxide has on the oxygen carrying capacity of the blood, we are also beginning to understand how carbon monoxide can effect the heart. As we will see later, carbon monoxide is a major risk factor for the development of coronary artery heart disease. While the reasons for this are varied, one major factor currently under intensive investigation is carbon monoxide exposure. Carbon monoxide will increase the rate for development of atherosclerosis, or hardening of the arteries, to the heart. This process decreases the amount of blood the heart receives, and can result in angina, or "heart pain". Additionally, when the blood supply becomes critically short, then an actual heart attack may result. When you stop smoking, many of these process we have just mentioned will reverse. With no more of that irritating cigarette smoke being breathed into the lungs, your bronchial airways will begin to recover, the amount of mucus or phlegm you produce will rapidly decrease, and loosen up. There will be less obstruction to movement of air in and out of your lungs as the irritated airways begin opening up again. The rate of decline of your lung function will no longer be about three times greater than nonsmokers, but the rate will return toward normal levels. That's the good news. a The bad news is that you years of smoking have probably done actual structural damage to your lungs which will never be fully repaired. You may have developed areas of emphysema where the alveoli have been destroyed leaving actual open spaces which are useless for breathing function. This function will simply not return. However, you can prevent your deteriorating lung function from getting any worse by stopping your smoking right now before any more permanent damage results. The extent to which your lung function improves after smoking cessation largely depends upon exactly how much of your lung disease is from emphysema or destroyed alveoli (which will not improve) or chronic bronchitis (which will show some improvement. Your physician may be able to give you pulmonary function tests and get at least an idea how much of your lung disease is due to emphysema or chronic bronchitis. But your best bet is to stop smoking right now before you develop symptoms. The pulmonary function test is a simple, quick and painless test that your doctor can perform to determine your degree, if any, of lung impairment. Recently, it has become apparent that even young adolescent smokers who have no apparent symptoms may still have abnormalities in their pulmonary function tests. Additionally, it is also possible that patients may have shortness of breath but have normal pulmonary function tests. Such would be the case in patients with significant deconditioning or heart disease. Also, if the pulmonary function tests shows that you do have obstruction lung disease, the physicians may order a bronchodilator be given.. The pulmonary function test is then repeated to see whether there has been any significant improvement after the bronchodilator treatment. It may then be possible to determine whether your type of lung disease will be helped by medications, as well as the severity of the underlying disease. Maybe if you see with your own eyes how your lungs are disease and performing less than they should be, you will become more inclined to stop breathing in so much smoke. Smoking not only damages your lungs, which is certainly easy to understand, but it may also severely damage your heart in ways you probably have not even contemplated. One of the more obscure but common ways that smoking can damage the heart is through its effects on the lungs. To understand this, we need to review a little (but not too much) of anatomy. Blood returns to the right side of the heart (the right atrium and right ventricle) before it can be pumped through the rest of the body. But the blood that is returned by this venous system to the right heart has been largely depleted of its oxygen and contains large amounts of carbon dioxide that must be eliminated. In order for the blood to absorb oxygen and discharge its carbon dioxide, it must first be pumped to the lungs. From the lungs, blood goes to the left heart (left atrium and left ventricle) where it is pumped in to the arterial system and the rest of the body. From the arterial system, blood enters the capillaries, discharges its oxygen into the tissues, picks up carbon dioxide as a waste produce, goes to the veins and then back again to the right heart. This circuit ensures a continuous flow of oxygen through the body, and allows carbon dioxide to be deleted. Naturally, with the heart pumping about five quarts of blood a minute, there is a pressure built up in the vessels. On the arterial system, the pressure is the common, familiar to everybody blood pressure that your physician measures with the familiar arm cuff. There is also a pressure in the venous system as blood is returned to the heart, and pressure as blood is pumped from the right heart to the lungs. The latter pressure (called the pulmonary artery pressure) is the one we must now closely examine. Blood that passes through the lungs generates a pressure that is proportional to the amount of blood pumped per minute, and the resistance to that flow. In other words, with greater resistance to the passage of blood through the lungs, the pressure that is produced increases tremendously. With lung disease, there is a tremendous increase in the resistance of the lung circulation of blood which means that the right heart must generate much larger pressure to get blood through. This can p7ut much strain on the right heart because it just was not designed to carry such increased pressure loads. The right heart may be able to withstand this pressure for short periods of time, but eventually it will fail, and just simply cannot pump enough blood to the lungs. To try to adapt the right heart may enlarge as it attempts to develop enough pumping pressure, but eventually things simply break down. When the right heart fails due to lung disease, a condition known to physicians as cor pulmonale has developed. The symptoms of cor pulmonale are many, and can be easily recognized by any physician. When the right heart fails, not enough blood gets to the left heart, the arterial blood pressure falls, and the patient begins to feel chronically tired and lethargic. The exercise tolerance decreases because the heart just cannot keep up with the demands placed upon it. Fluid tends to accumulate because the right heart cannon pump it fast enough to the left heart. This results in swelling or "edema' primarily of the ankles and legs. Edema makes the legs and ankles much more prone to ulcerations and infections, and can be very uncomfortable. Your physician can diagnose cor pulmonale many ways, including by an electrocardiogram (EKG), chest X-rays, physical examination, and radionuclide studies. You certainly should stop smoking before your lung disease becomes so severe that your right heart is affected, producing potentially life threatening cor pulmonale. Many smokers may not feel too threatened (despite all of the previous discussion) with their own health. Perhaps they are already senior citizens and have been lucky enough thus far to escape the ravages of smoking-related pulmonary diseases. Often, more senior individuals are then lulled into a false security with their mistaken belief that they now have it made. They may be partially right in that their chance of acquiring severe obstructive pulmonary disease is significantly reduced if they have normal pulmonary function in old age. Of course, these individuals still have plenty of time to develop lung cancer or significant coronary artery heart disease. But perhaps one of the more compelling arguments to these people to stop smoking is that even if they are not concerned enough about their own health, they should consider the health consequences to their family and associates. Now, I do not just mean the uncomfortable annoying necessity of them having to be constantly exposed to exhaled tobacco smoke, but also the recently described very real pulmonary damage that may result from their exposure. This is called "passive smoking", of the exposure to tobacco smoke that non-smokers get just by being in the vicinity of smokers. Recently, studies have been showing that this passive smoking exposure to cigarette smoke may be more than just annoying to the non-smoker. Let's now examine how your cigarette smoking may actually prove damaging to your associates and loved ones. Asthma is a lung condition that is similar in some respects to the obstructive lung diseases we have examined previously - emphysema and chronic bronchitis. It is different in other respects however. One of the major differences is that it is usually completely or largely reversible at times, and that it can be present inyoung people and children who have obviously never smoked previously. It is certainly true that if anyone in your family or associates in the work-place has asthma, they will be very bothered by your cigarette smoke, even if they are polite enough to tolerate you. Cigarette smoke is a very powerful irritant to the airways, and can easily provoke an episode of bronchospasm or acute asthma attack. Also, if your associates have chronic bronchitis or smphysema, they will also be very appreciative of your not smoking. They have come to appreciate what it is like to breath again, enjoy good food, and not be constantly winded with the least exertion. Being forced to breath your smoke may cause them discomfort if the smoke irritates their airways too. If an associate of yours has heart disease, then your smoke may also prove quite irritating, the smoke from your cigarette contains high concentrations of carbon monoxide which can build to quite significant levels in a poorly ventilated room. When this occurs, your friend with coronary artery heart disease may have oxygen displaced from hemogloven by carbon monoxide, producing an acute anginal episode or even a heart attack. What has recently become increasingly evident is the effect smoking
has on young children. If you are pregnant, you must stop smoking.
Your unborn baby will be deprived of oxygen every time you light up.
Infants born of mothers who smoke have a significantly higher perinatal
death rate than others. But that is not all. If your infant
has survived its birth trauma, then it has to breath your cigarette smoke
day in and day out. There is recent evidence that strongly suggests
that this constant exposure may produce more childhood colds and lung infections,
which may produce significant lung disease lasting into adulthood.
The most common cause of death in America today is heart disease, and smoking is one of the major risk factors for its development. Pure and simply, if people stopped smoking, they would have a marked reduction in their chances of developing heart disease. As a matter of fact, the decrease in heart attack mortality in America since 1964 has been at least partially contributed toa reduction in the smoking habit. How does smoking produce so much damage to the heart? Let's examine the issue. Coronary artery disease is a very complex phenomenon that is only partially understood. Basicaly, there is a reduction in blood flow to the heart that is caused by narrowing of the arteries supplying the heart - the coronary arteri3es. In Americans, autopsy results show that evidence for early coronary artery disease begins early, sometime even in adolescent years. There is increased deposition of cholesterol and other lipids (fats) into the vessel wall, along with other pathologic changes which produce a narrowing of the vessel. When this narrowing becomes severe enough, then the blood flow is reduced first with exercise, and then at rest, producing pain - or "angina". In some patients, the vessel wall may, for reasons that are not entirely clear, develop spasm which can further narrow this opening. Additionally, platelets appear to be involved. Platelets are very small structures in blood which are instrumental in blood clotting. When stimulated by any of a large number of chemical substances or physical trauma, they become sticky and adhere to each other. When this happens enough, a platelet plug can form. Usually this plug serves us well by helping to stop bleeding from cut vessels. But the plug may form in an already narrowed vessel, such as a diseased coronary artery, and totally obstructs blood flow. This can initiate a heart attack and possibly kill the patient. These three factors, coronary artery spasm, deposition of fats
with or without calcification, and platelet pluts - produce the vast majority
of heart disease. The precise mechanisms as to how these three components
all interact is still not entirely clear, but is an active area of intensive
medical research. What has become evident, however, is how bad smoking
is for the heart. Smoking increases the platelet aggregations making
them plug more easily, increases the rate of atherosclerosis, and can cause
spasm of the arteries. Even if a thin trickle of blood can manage
to get past an obstruction in a coronary artery, the blood is not carrying
as much oxygen as it could due to inhaled carbon monoxide. Also,
smoking forces the heart to work much harder by increasing the blood pressure
and elevating the heart rate. The only mystery concerning heart disease
and smoking is that more people are not dying.
This is a very dangerous situation. The tissues are becoming
starved for blood, oxygen, and nutrients, and will simply die if the obstruction
is nor somehow relieved. This can result in ulceration (which almost
inevitably become infected) and gangrene (which may require amputation).
Summary of Medical Facts Concerning Smoking This brief overview has given us an idea as to how devastating tobacco smoking can be to the health of the smoker. Smoking may severely affect the lungs, producing emphysema, chronic bronchitis, and lung cancer. Smoking will produce dangerous carbon monoxide which will displace oxygen from the hemoglobin in our red blood cells, thereby reducing oxygen delivery to our tissues, maybe even to dangerous levels. Smoking can severely damage the heart by forcing it to work much harder while reducing its blood supply. Additionally, smoking may encourage the development of disease in arteries leading to "claudication" or leg pain with exercise. cigarette smoking is a large factor in the development of these ravaging diseases. Isn't it time you stopping smoking - today? Stop smoking now, if not for yourself, then for your family and loved ones. They want you around, and they want you as a person, and not as an invalid, bed bound on oxygen tanks. |