Introduction
People have always questioned the effects of cigarette smoking. While smokers definitely gain something out of it, non-smokers are concerned with the risks it poses on human health. Smoking not only affects the smoker’s health but also those who are exposed to the smoke it generates. In the United States alone, cigarette smoking is responsible for up to 430,000 deaths annually (Ockene and Miller, 1997). The many health risks of cigarette smoking is recognized by health experts and governments worldwide, but further clinical and empirical researches have continuously shown that passive smoking presents the same, if not worse, health risks as active smoking.
Cigarette smoking is considered to be the single, most preventable cause of death in the United States and in many countries. Cigarettes contain about 4,000 chemical agents, about 60 of which are carcinogens—cancer causing chemicals. Many of the substances found in cigarettes such as carbon monoxide, tar, arsenic and lead are toxic to the human body. Perhaps the most harmful of these substances is nicotine, a drug that is naturally present in tobacco plants and functions as an anti-herbivore chemical. Nicotine is highly toxic that it has been used as pesticide in the past. In low concentrations, however, nicotine has desirable effects including increasing alertness, an aid to relaxation, as antidepressant, and reducing positive symptoms such as hallucinations. An average cigarette contains about 10 milligrams of nicotine and is primarily responsible why smokers become addicted to cigarettes. The American Heart Association has referred to nicotine addiction as historically “one of the hardest addictions to break.”
Why People Choose to Smoke
People smoke for many different reasons. While for some it is for fun and a way to enjoy a moment of pleasure away from the troubles of life, for others it is a way to relax and makes them think more clearly. It gives a legitimate excuse to linger a little longer after meals, to stop working for a few minutes, or to just sit back and do nothing other than smoking. Some smoke when they need a break or a moment for themselves. Smoking also provides a means to block outside distractions such that some argue that moderate smoking stimulate mental alertness (Dichter, 1947). This may be attributed to the fact that nicotine has the capability of increasing alertness, which may in turn enhance concentration. Many smokers claim that smoking helps them cope with stress. Smoking is also an ersatz activity—that is, people will often pass the time from waiting through smoking. Some smoke when they feel bored or lonely. It gives the smoker’s hands something to do which may otherwise cause self-consciousness or interfere with mental activities. Smoking has a psychotherapeutic effect from which it helps people relax during the unpleasant circumstance of waiting, particularly in cases where they wish they could do something but are unable to do so and from which causes an attack of nervous anxiety. The relaxing effect of nicotine is again responsible for this. Smoking also provides relief in times of great tension. Smoking can also relieve a person from “mental depression by forcing a rhythmic expansion of the breast and thus restoring the normal pace of breathing” (Dichter, 1947). As it allows a person to breathe more steadily, smoking also has the capability to calm a person down especially when that person is enraged. Smoking has been proven as a powerful support tool when things go wrong. The antidepressant effect of nicotine makes these all possible.
Cigarette smoking also often helps in breaking social barriers and in making friends with other people. Smoking has the same effect as drinking. It is a way to start conversation and meet new people. Most people enjoy smoking with others as a shared activity. Smoking also helps people look more confident and in control of themselves and their surroundings. Others also smoke due to the belief that smoking helps them reduce weight.
The Adverse Effects of Smoking on the Smoker
While smoking is definitely a form of pleasure, it has many adverse effects on the smoker. Because cigarettes contain nicotine, cigarette smoking is highly addictive; so addictive, in fact, that smokers who had a better thought of it find it difficult to quit. It works much the same way as a heroin or cocaine. It takes only 10 seconds from the time it was inhaled for nicotine to reach the brain and trigger the release of dopamine—a chemical that is linked to the feeling of pleasure. Smoking is so highly addictive that there are times when a smoker does not particularly want to smoke, but will feel that he or she too will have to smoke when he or she sees someone who is smoking. Sometimes, even the mere mention or picture of smoking or cigar will compel a smoker to smoke. Smokers confess that there is an immense yearning for cigarette whenever they are forced to abstain for some time and for any given reason.
The association of cigarette smoking to chronic lung diseases such as asthma, emphysema, and chronic bronchitis has been repeatedly shown. Active cigarette smoking is the major known cause of lung cancer, which is identified as the most frequently occurring cancer in the world, accounting with up to 1.2 million diagnosed cases in 2000 (Taylor et al, 2007). Cigarette smoking can also cause cardiovascular diseases, strokes, and cataracts. Cigarette smoking is responsible for a wide range of cancer including that of the larynx, oral cavity and pharynx, esophagus and bladder, as well as those of the kidneys, pancreas, cervix, and stomach. It is also associated for up to 87 percent of deaths from lung cancer alone and up to 30 percent of all cancer deaths. Cigarette smoking also causes acute myeloid leukemia and acute eosinophilic pneumonia. It is also being associated to tooth loss among young adults. In fact, cigarette smoking is shown to affect almost every major organ in the human body.
The epidemiological evidence of the risks of active smoking on cardiovascular disease is overwhelming. It has been shown that the risk of death from coronary heart disease is elevated at least two-fold among smokers and about 30 percent of deaths from coronary heart disease are attributable to cigarette smoking (Ockene and Miller, 1997). Two-thirds of sudden cardiac death cases that are due to acute coronary thrombosis occur among smokers (Raupach et al., 2005). Smoking has been demonstrated to impair endothelial function, through the use of laboratory animals as test subjects. Observations in clinical studies have also found that the earliest sign of endothelial dysfunction among smokers is the impairment of endothelium-dependent vasorelaxation and that smoking inhibited endothelium-dependent vasodilatation (Raupach et al., 2005). Because of its function in blood circulation, impairments in vasorelaxation and vasodilatation increase the blood pressure, thereby increasing the risks of heart diseases. Active smoking is also thought to elicit an adrenal epinephrine release which has the capacity to enhance platelet activation (Raupach et al., 2005). Platelet activation plays a crucial role in the pathophysiology of acute coronary syndrome.
Robbins et al. (1994) reported that there is a linear increase in risk for strokes between those who never smoked and those who currently smokes 20 or more sticks of cigarettes per day. Their data reveal that heavy smokers have up to 2.71 times the risk of nonfatal stroke compared to those who never smoke. Robbins et al. (1994) explained that the association between cigarette smoking and stroke is attributable through several mechanisms. Smoking is regarded to decrease the level of high-density lipoprotein cholesterol and can increase hematocrit, changes associated with an increased risk for stroke. Experiments have also revealed that smoking can cause direct endothelial damage which is an essential component to atherosclerosis, a process which slowly progresses into stroke.
In pregnant women, cigarette smoking “significantly increases the risks of spontaneous abortion and of preterm or low weight delivery” (Dollberg et al., 2000). Maternal smoking also causes fetal growth restriction in the third trimester. It is also associated with some neonatal morbidity including neonatal asphyxia, intraventricular hemorrhage, reduced lung function, and increased incidence of perinatal death or sudden infant death syndrome. Maternal smoking also increases the risk of neuro-developmental impairment during later childhood. Furthermore, smoking during pregnancy reduced the number of haematopoietic progenitor cells in the umbilical vein blood of the newborn (Raupach et al., 2005).
Even when active tobacco smoking has been continuously shown to increase health risks, most people continue to smoke, perhaps because of the benefits they gain from smoking. Clinical data also reveal that the increase in the risk factor depends on different factors: the number of cigarettes being smoked in a day, the intensity of the intake, i.e. the frequency and length of inhalation, the age at which smoking has begun, and the number of years a person has smoked.
On the other hand, smokers tend to have a feeling of guilt with regards to smoking—a sign that most believe that cigarette smoking is immoral. Most smokers worry that they are smoking too much and strive to cut down on the number of sticks they light up a day. Other smokers try to periodically abstain from smoking to minimize its adverse effects and prove to themselves that they could still do without smoking. These efforts to minimize smoking may reveal that smokers are also aware of the adverse effects of smoking, have respect to the majority who are non-smokers, and are willing to sacrifice the feeling of pleasure from smoking to assuage the feeling of guilt. However, Dichter (1947) explained that “the mind has a powerful influence on the body, and may produce symptoms of physical illness. Guilt feelings may cause harmful physical effects not at all caused by the cigarettes used, which may be extremely mild. Such guilt feelings alone may be the real cause of the injurious consequences.”
Adverse Effect of Secondhand Smoking
Not only does cigarette smoking affect the health of those who smoke themselves, but also those who are exposed to the smoke. The smoke given off by the burning end of a cigarette, called sidestream smoke and accounting for 85 percent of the total secondhand smoke, and the smoke being exhaled off by smokers, called the mainstream smoke, are involuntarily inhaled by people who do not smoke. These smokes are termed as Environmental Tobacco Smoke (ETS) or, simply, secondhand smoke. Secondhand smoke lingers for hours even after the cigar has been extinguished. Furthermore, the toxins found in sidestream smoke are 100-fold more concentrated than those found in the mainstream smoke, underscoring the potential impact of secondhand smoke on human health. Passive smoking is the term used to refer to the exposure to secondhand smoke by people who do not themselves smoke.
Passive smoking causes a wide range of adverse health effects particularly by causing or aggravating the instance of asthma and other respiratory infections. Passive smoking is also associated with the increase in the incidence of cardiovascular disease, lung cancer, and fetal hypoxia. The Environmental Protection Agency has classified passive smoking as a known cause of cancer in humans. Even short exposures to secondhand smoke also potentially increases the risks of heart attacks as it causes blood platelets to become stickier, damage the lining of the blood vessels, decrease the coronary flow velocity reserves and reduce heart rate variability.
In the United States alone, secondhand smoke is responsible for 50,000 deaths of adult non-smokers each year. It is also responsible for approximately 300,000 cases of lower respiratory tract infections in infants and children under 18 months old, and causes up to 400 cases of sudden infant death syndrome annually. These data are retrieved still in the United States alone. It is estimated that passive smoking increases the overall risk of an acute cardiovascular event by up to 35 percent and that the risk of acute coronary syndromes can reach up to 97 percent in people who are exposed to secondhand smoke in their homes (Raupach et al., 2005). Passive smoking also increases the risk of coronary heart disease by 25 percent among non-smokers and environmental tobacco smoke is being accounted for 5,500 deaths from coronary heart disease in the United Kingdom and up to 62,000 coronary heart disease deaths in the United States (Heidrich et al, 2007).
The Evidences against the Dangers of Passive Smoking
Researches have been performed to study the effects of second-hand smoking. Although the chemical components of tobacco smoke actively inhaled by smokers are different to those passively inhaled by non-smokers, the toxic and carcinogenic effects are similar.
Perhaps the most common and the most persistent health risk being associated to passive smoking is lung cancer and other respiratory tract infections and diseases. Environmental tobacco smoke has been classified by the US Environmental Protection Agency as a known human lung carcinogen since 1993 and “has been the most widely studied risk factor of lung cancer among non-smokers” (Taylor et al., 2007). Benzo[a]pyreane diol epoxide, a substance that shows a direct aetiological association with lung cancer, is found in environmental tobacco smoke (Taylor et al., 2007). A study conducted calculated a pooled estimate of relative risk of lung cancer associated with the exposure to environmental tobacco smoke (Taylor et al., 2007). These data came from a pool of women who had never smoked but are married to smokers and are therefore exposed to secondhand smoke. Their analysis reinforced a previous but recently published study showing a 27 percent excess in risk of lung cancer among women who never smoked but are exposed to secondhand smoke through their spouses compared to women who never smoked and are not exposed to secondhand smoke. This study concluded that the abundance of evidence and the consistency of findings “overwhelmingly support the existence of a causal relationship between passive smoking and lung cancer” (Taylor et al., 2007).
Sandler, Everson, and Wicox (1985) studied the risk of developing cancer for passive smokers by obtaining information on cancer patients and non-cancer controls and found that the cancer risk among individuals that has been or currently married to smokers was 1.6 times than those who were never married to smokers. The patients in the study, included not only those with lung cancer, but included patients with cancer from all sites except that of basal cell and the increased risks were seen for several specific cancer sites including those that were not previously held to be related to smoking. This implies that passive smoking not only provides a risk in lung cancer but in a wide range of cancers. Furthermore, Sandler, Everson, and Wicox (1985) reported that the risks in cancer from passive smoking appear to be greater in groups who are generally at lower cancer risks, i.e., females, non-smokers, and individuals younger than the age of 50.
There are compelling evidences that passive smoking is associated with coronary heart diseases and cardiovascular diseases. It has been shown that the risk of having coronary heart disease increases by as much as 25 percent in non-smokers who are exposed to environmental tobacco smoke. In 1998, a study conducted found that “passive smoking turns the acetylcholine-induced coronary artery relaxation into a vasoconstriction in women” (Sumida et. al., 1998). Another study has shown that exposure to nicotine damages and causes increased permeability of endothelial cells (Raupach et al., 2005). It has also been shown that at concentrations equivalent to its level in smokers, cotinine, a metabolite of nicotine, suppresses the growth of haematopoietic progenitor cells. These cells, which have the potential to differentiate into mature endothelial cells, are necessary for the regeneration of vascular endothelial layers and restoration of endothelial function which are of central importance for vascular homeostasis and atherothrombosis prevention. Atherothrombosis is a condition that is regarded to be the major cause of acute coronary syndromes that progresses to “coronary artery disease, myocardial infarction, ischemic stroke, transient ischemic attack, peripheral arterial disease and vascular death” (Vilez-Gonzalez, Fuster, and Badimon, 2004). Research has also found that 20 minutes of being passively exposed to whole smoke is sufficient to induce platelet activation comparable to that of actively smoking one or two sticks of cigarettes (Raupach et. al., 2005). A research conducted hypothesized that “once an acute coronary syndrome occurs, the resulting damage to the heart might further be aggravated by ongoing passive smoking” (Raupach et al., 2005).
Exposure to environmental tobacco smoke also increases the risk of stroke. A group of researches studied the risk factor on ischemic stroke from first-episode patients (patients who have been diagnosed of ischemic stroke for the first time) and found that the risk of stroke is twice as high in patients whose spouses smoked than with those whose spouses did not (You et. al., 1999). In another study, the effects of chronic cigarette smoking on cerebral blood flow was investigated and smoking was found to be a potent risk factor in decreasing blood flow suggesting an increased risk for stroke (Rogers et al., 1983) Chronic cigarette smoking of persons with other risk factors, i.e., hypertension, hyperlipidemia, diabetes mellitus, and heart disease, further reduced cerebral blood flow compared to those who had other risk factor but did not smoke.
Shaul Dollberg et al. (2000) evaluated whether the absolute nucleated red blood cell (RBC) count is elevated in infants born to women who were exposed to second-degree smoking during pregnancy. They compared the absolute nucleated RBC counts taken during the first 12 hours in two groups of term, normally delivered infants and found that the median absolute nucleated RBC count is higher in the “passive smoking” group than the “non-smoking” control group. “Passive smoking” group include infants whose mothers were routinely exposed to second-degree smoke in home or office while the “non-smoking” include infants whose mothers have not been routinely exposed to any cigarette smoke. None of the subjects were infants of women with conditions known to increase nucleated RBC counts. An increase in the absolute nucleated RBC count is associated with hypoxic injuries—injuries related to the inadequate oxygenation of the blood—and the result the study reveals that exposure to second-degree tobacco smoke during pregnancy may have serious implications to the unborn child.
Although researches have been performed on the risks of passive smoking to human health, estimation of affected cases is a complex procedure, much more with estimating the number of deaths attributable to passive smoking. This is because there are multiple settings of exposure (i.e., home, workplace, and public places such as at bars and restaurants), different reported relative risks, and different class of population at risk (i.e., men, women, children, never smokers, former smokers and current smokers). Nevertheless, clinical and empirical data reveal a substantial association between health risks and exposure to environmental tobacco smoke.
Benefits of Quitting Smoking
Given the health risks of active and passive smoking, quitting cigarette smoking would most definitely minimize, if not totally eradicate, these risks. Empirical data reveals that cases of illnesses and diseases significantly drop when people quit smoking, either voluntarily or with the aid of legislation. Even former smokers who have been into many years of heavy smoking are revealed to still benefit from quitting.
Following the enactment of a local law prohibiting smoking in public and workplaces, hospital admissions for acute myocardial infarction has dropped by 40 percent (Raupach et. al., 2005). Investigations have also revealed a substantial decrease in coronary heart disease mortality for those who quit smoking than with those who continue to smoke. There is as much as 50 percent reduction in risk of re-infarction, sudden cardiac death, and total mortality for former smokers who have been diagnosed with coronary heart disease while they were into cigarette smoking (Ockene and Miller, 1997).
Conclusion
Smoking has many adverse effects not only on the health of smokers but also on the health of those who do not smoke but are exposed to secondhand smoke. Scientific and health experts regard smoking as the single, most preventable cause of death and governments strive to minimize smoking and its adverse effects by passing legislations that prohibit smoking in public areas or by increasing state taxes for tobacco products, thereby making them more expensive and less accessible to people. Quitting cigarette smoke has been proven to reverse the risks acquired from smoking, aside of course from contributing to minimize environmental tobacco smoke.
While smoking provides many benefits such as being a form of pleasure and a way to relax, it has many adverse effects. Actively smoking tobacco products, cigarettes in particular, is considered as the major cause of lung cancer. However, various clinical and empirical research show that cigarette smoking is also a risk factor to a wide range of cancer cases, may it be previously related to smoking or not. Cigarette smoking is also being attributed to a wide range of respiratory tract infections and diseases. Cigarette smoking is also associated with an increased risk in cardiovascular and coronary heart diseases, as well as ischemic stroke. Furthermore, actively smoking during pregnancy poses health risks not only to the smoking mother but also to the unborn child or children. It increases the risk of spontaneous abortion, causes preterm and a low-weight birth, increases neonatal morbidity, increases the risk of neuro-developmental impairment during later childhood, and increases the instance of sudden infant death syndrome.
The smoke coming off of a cigarette and the smoke being exhaled by smokers also poses a threat even to those who do not smoke. The causal relationship between passive smoking and lung cancer has been continuously shown. The toxic and carcinogenic content of mainstream smoke coupled with its higher concentrations in sidestream smoke, which comprises 85 percent of the total secondhand smoke, poses a great risk in developing cancer of any kind to those who are exposed to it, regardless of whether they are routinely exposed or have been exposed for a short term. There are substantial epidemiological evidences linking exposure to secondhand smoke to cardiovascular diseases. Exposure to secondhand smoke appears to be capable of precipitating the atherothrombosis—the acute manifestation of cardiovascular diseases—and may also have a negative impact on the outcome of patients who suffer acute coronary syndromes. Clinical and experimental researches have exposed the acute effects of passive smoking, including impairments in the endothelial function, platelet activation, oxidative stress and inflammatory reactions—all involved in the pathogenesis of atherosclerosis. Exposure to secondhand smoke also decreases cerebral blood flow, which in turn incites ischemic stroke. Clinical data reveal that the risk of stroke is twice as high in patients exposed to secondhand smoke through spouses who are smokers. Exposure to secondhand smoke during pregnancy also increases the risk of sudden infant death syndrome or might increase the absolute nucleated red blood cell count of the infants which causes hypoxic injuries.
Considering the adverse effects of active and passive smoking, it is only fair that the government must take steps into minimizing, if not to totally eradicate, tobacco smoking in general. The benefits obtained from quitting smoking far outweigh the benefits and pleasure obtained from smoking; not only for the smoker alone, but also for others who do not smoke but are constantly put in risk of the dangers caused by smoking.
References
Dichter, E. (1947). Why do we smoke cigarettes? Retrieved February 27, 2008, from http://smokingsides.com/docs/whysmoke.html
Dollberg, S., Feinaru, O., Mimouni, F. B., Shenhav, M., Lessing, J. B., and Kupferminc, M. (2000). Effect of passive smoking in pregnancy on neonatal nucleated red blood cells. Pediatrics, Vol. 106, No. 3.
Heidrich, J., Wellmann, J., Heuschmann, P. U., Kraywinkel, K., and Keil, U. (2007). Mortality and morbidity from coronary heart disease attributable to passive smoking. European Heart Journal Vol. 28, No. 20, 2498-2502.
Ockene, I. S., and Miller, N. H. (1997). Cigarette smoking, cardiovascular disease, and stroke: A statement for healthcare professionals from the American Heart Association. Circulation No. 96, 3243-3247.
Raupach, T., Schafer, K., Konstantinides, S., and Andreas, S. (2005). Secondhand smoke as an acute threat for the cardiovascular system: A change in paradigm. European Heart Journal Vol. 27, No., 4, 386-392.
Robbins, A. S., Manson, J. E., Lee, I., Satterfield, S., and Hennekens, C. H. (1994). Cigarette smoking and stroke in a cohort of U.S. male physicians. Annals of Internal Medicine Vol. 120, No. 6, 458-462.
Rogers, R. L., Meyer, J. S., Shaw, T. G., Mortel, K. F., Hardenberg, J. P., and Zaid, R. R. (1983). Cigarette smoking decreases cerebral blood flow suggesting increased risk for stroke. The Journal of the American Medical Association Vol. 250, No. 20, 2796-2800.
Sandler, D. P., Everson, R. B., and Wicox, A. J. (1985). Passive smoking in adulthood and cancer risk. American Journal of Epidemiology Vol., 121, No. 1, 37-48.
Sumida, H., Watanabe, H., Kugiyama, K., Ohgushi, M., Matsumura, T., and Yasue, H. (1998). Does passive smoking impair endothelium-dependent coronary artery dilation in women? Journal of the American College of Cardiology Vol. 32, 811-815.
Taylor, R., Najafi, F., and Dobson, A. (2007). Meta-analysis of studies of passive smoking and lung cancer: Effects of study type and continent. International Journal of Epidemiology Vol. 35, No. 5, 1048-1059.
Viles-Gonzalez, J. F., Fuster, V., and Badimon, J. J. (2004). Atherothrombosis: A widespread disease with unpredictable and life-threatening consequences. European Heart Journal Vol. 25, No. 14, 1197-1207.
You, R. X., Thrift, A. G., McNeil, J. J., Davis, S. M., and Donnan, G. A. (1999). Ischemic stroke risk and passive exposure to spouses’ cigarette smoking. American Journal of Public Health Vol. 89, No. 4, 572-575.
