cigarette smoking conclusion essay

Essay on Smoking

500 words essay on smoking.

One of the most common problems we are facing in today’s world which is killing people is smoking. A lot of people pick up this habit because of stress , personal issues and more. In fact, some even begin showing it off. When someone smokes a cigarette, they not only hurt themselves but everyone around them. It has many ill-effects on the human body which we will go through in the essay on smoking.

Ill-Effects of Smoking

Tobacco can have a disastrous impact on our health. Nonetheless, people consume it daily for a long period of time till it’s too late. Nearly one billion people in the whole world smoke. It is a shocking figure as that 1 billion puts millions of people at risk along with themselves.

Cigarettes have a major impact on the lungs. Around a third of all cancer cases happen due to smoking. For instance, it can affect breathing and causes shortness of breath and coughing. Further, it also increases the risk of respiratory tract infection which ultimately reduces the quality of life.

In addition to these serious health consequences, smoking impacts the well-being of a person as well. It alters the sense of smell and taste. Further, it also reduces the ability to perform physical exercises.

It also hampers your physical appearances like giving yellow teeth and aged skin. You also get a greater risk of depression or anxiety . Smoking also affects our relationship with our family, friends and colleagues.

Most importantly, it is also an expensive habit. In other words, it entails heavy financial costs. Even though some people don’t have money to get by, they waste it on cigarettes because of their addiction.

How to Quit Smoking?

There are many ways through which one can quit smoking. The first one is preparing for the day when you will quit. It is not easy to quit a habit abruptly, so set a date to give yourself time to prepare mentally.

Further, you can also use NRTs for your nicotine dependence. They can reduce your craving and withdrawal symptoms. NRTs like skin patches, chewing gums, lozenges, nasal spray and inhalers can help greatly.

Moreover, you can also consider non-nicotine medications. They require a prescription so it is essential to talk to your doctor to get access to it. Most importantly, seek behavioural support. To tackle your dependence on nicotine, it is essential to get counselling services, self-materials or more to get through this phase.

One can also try alternative therapies if they want to try them. There is no harm in trying as long as you are determined to quit smoking. For instance, filters, smoking deterrents, e-cigarettes, acupuncture, cold laser therapy, yoga and more can work for some people.

Always remember that you cannot quit smoking instantly as it will be bad for you as well. Try cutting down on it and then slowly and steadily give it up altogether.

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Conclusion of the Essay on Smoking

Thus, if anyone is a slave to cigarettes, it is essential for them to understand that it is never too late to stop smoking. With the help and a good action plan, anyone can quit it for good. Moreover, the benefits will be evident within a few days of quitting.

FAQ of Essay on Smoking

Question 1: What are the effects of smoking?

Answer 1: Smoking has major effects like cancer, heart disease, stroke, lung diseases, diabetes, and more. It also increases the risk for tuberculosis, certain eye diseases, and problems with the immune system .

Question 2: Why should we avoid smoking?

Answer 2: We must avoid smoking as it can lengthen your life expectancy. Moreover, by not smoking, you decrease your risk of disease which includes lung cancer, throat cancer, heart disease, high blood pressure, and more.

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Essay on Smoking Cigarettes

Students are often asked to write an essay on Smoking Cigarettes in their schools and colleges. And if you’re also looking for the same, we have created 100-word, 250-word, and 500-word essays on the topic.

Let’s take a look…

100 Words Essay on Smoking Cigarettes

Harmful habit.

Smoking cigarettes is a dangerous habit that can lead to many health issues. The chemicals in cigarettes damage the lungs and heart, and they can also cause cancer.

Effects on the Lungs

Smoking cigarettes paralyzes the tiny hairs in the lungs that help to keep them clean. This makes it easier for tar and other harmful substances to build up in the lungs, which can lead to lung disease and cancer.

Effects on the Heart

Smoking cigarettes increases the risk of heart disease and stroke. The chemicals in cigarettes damage the blood vessels and make them more likely to form clots. Smoking also raises blood pressure and cholesterol levels, which are both risk factors for heart disease.

Effects on Cancer

Smoking cigarettes is the leading cause of preventable cancer deaths. The chemicals in cigarettes can damage DNA and cause cells to grow out of control. Smoking cigarettes increases the risk of cancer of the lungs, mouth, throat, esophagus, stomach, pancreas, kidney, and bladder.

250 Words Essay on Smoking Cigarettes

Smoking cigarettes: a harmful habit.

Smoking cigarettes is a habit that can have serious consequences for your health. Cigarettes contain harmful chemicals that can cause cancer, heart disease, and other health problems.

Smoking cigarettes is the leading cause of preventable cancer deaths. Cigarettes contain chemicals that can damage the DNA in your cells, which can lead to cancer. The chemicals in cigarettes can also cause inflammation, which is a risk factor for cancer.

Heart Disease

Smoking cigarettes increases your risk of heart disease. The chemicals in cigarettes can damage the blood vessels in your heart, which can lead to a heart attack or stroke. Smoking cigarettes can also raise your blood pressure and cholesterol levels, which are also risk factors for heart disease.

Quitting Smoking

If you smoke cigarettes, quitting is the best thing you can do for your health. Quitting smoking can reduce your risk of cancer, heart disease, and other health problems. It can also improve your appearance, energy levels, and overall quality of life.

There are many resources available to help you quit smoking. Talk to your doctor, pharmacist, or other healthcare provider. You can also find support and information online or through quit-smoking programs.

Smoking cigarettes is a harmful habit that can have serious consequences for your health. If you smoke, quitting is the best thing you can do for your health. There are many resources available to help you quit smoking.

500 Words Essay on Smoking Cigarettes

What are cigarettes.

Cigarettes are small, cylindrical objects made of tobacco leaves that are rolled in paper. They are lit at one end and smoked, with the smoke being inhaled into the lungs.

Why Do People Smoke?

There are many reasons why people start smoking cigarettes. Some people think it looks cool, while others believe it helps them to relax or concentrate. Still others may smoke because they are addicted to nicotine, a chemical found in tobacco that can make people feel good.

The Dangers of Smoking

Smoking cigarettes is a very dangerous habit. It can cause a number of health problems, including lung cancer, heart disease, and stroke. Smoking can also increase the risk of developing other diseases, such as COPD, emphysema, and bronchitis.

The Effects of Smoking on the Body

When you smoke a cigarette, the nicotine in the tobacco quickly enters your bloodstream. This can cause your heart rate and blood pressure to increase, and it can also make you feel lightheaded or dizzy. Smoking can also damage your lungs and other organs, and it can lead to a number of health problems.

If you smoke cigarettes, the best thing you can do for your health is to quit. Quitting smoking can be difficult, but it is possible. There are many resources available to help you quit, such as support groups, counseling, and medication.

Smoking cigarettes is a harmful habit that can lead to a number of health problems. If you smoke, the best thing you can do for your health is to quit. There are many resources available to help you quit, so there is no reason to continue smoking.

That’s it! I hope the essay helped you.

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Happy studying!

Secondhand Smoke Exposure and Cardiovascular Effects: Making Sense of the Evidence (2010)

Chapter: 8 conclusions and recommendations, 8 conclusions and recommendations.

In this report, the committee has examined three relationships in response to its charge (see Box 8-1 for specific questions):

The association between secondhand-smoke exposure and cardiovascular disease, especially coronary heart disease and not stroke (Question 1).

The association between secondhand-smoke exposure and acute coronary events (Questions 2, 3, and 5).

The association between smoking bans and acute coronary events (Questions 4, 5, 6, 7, and 8).

This chapter summarizes the committee’s review of information relevant to those relationships; presents its findings, conclusions, and recommendations on the basis of the weight of evidence; and presents its responses to the specific questions that it was asked in its task.

SUMMARY OF REPORT

Exposure assessment.

To determine the effect of changes in exposure to secondhand smoke it is necessary to quantify changes in epidemiologic studies. Airborne measures and biomarkers of exposure to secondhand smoke are available; they are complementary and provide different information (see Chapter 2 ). Biomarkers (such as cotinine, the major proximate metabolite of nicotine) in-

tegrate all sources of exposure and inhalation rates, but cannot identify the place where secondhand-smoke exposure occurred and, because of a short half-life they reflect only recent exposures. Airborne measures of exposure can demonstrate the contribution of different sources or venues of exposure and can be used to measure changes in secondhand-smoke concentrations at individual venues, but they do not reflect the true dose. Airborne concentration of nicotine is a specific tracer for secondhand smoke. Particulate matter (PM) can also be used as an indicator of secondhand-smoke exposure, but because there are other sources of PM it is a less specific tracer than nicotine. The concentration of cotinine in serum, saliva, or urine is a specific indicator of integrated exposure to secondhand smoke.

Although in most of the smoking-ban studies the magnitude, frequency, and duration of exposures that occurred before a ban are not known, monitoring studies demonstrate that exposure to secondhand smoke is dramatically reduced in places that are covered by bans. Airborne nicotine

and PM concentrations in regulated venues such as workplaces, bars, and restaurants decreased by more than 80% in most studies; serum, salivary, or urinary cotinine concentrations decreased by 50% or more in most studies, probably reflecting continuing exposures in unregulated venues (for example, in homes and cars).

Pathophysiology

The pathophysiology of the induction of cardiovascular disease by cigarette-smoking and secondhand-smoke exposure is complex and undoubtedly involves multiple agents. Many chemicals in secondhand smoke have been shown to exert cardiovascular toxicity (see Table 3-1 ), and both acute and chronic effects of these chemicals have been identified. Experimental studies in humans, animals, and cell cultures have demonstrated effects of secondhand smoke, its components (such as PM, acrolein, polycyclic

aromatic hydrocarbons [PAHs], and metals), or both on the cardiovascular system (see Figure 3-1 for summary). Those studies have yielded sufficient evidence to support an inference that acute exposure to secondhand smoke induces endothelial dysfunction, increases thrombosis, causes inflammation, and potentially affects plaque stability adversely. Those effects appear at concentrations expected to be experienced by people exposed to secondhand smoke.

Data from animal studies also support a dose–response relationship between secondhand-smoke exposure and cardiovascular effects (see Chapter 3 ). The relationship is consistent with the understanding of the pathophysiology of coronary heart disease and the effects of secondhand smoke on humans, including chamber studies. The association comports with known associations between PM, a major constituent of secondhand smoke, and coronary heart disease.

Overall, the pathophysiologic data indicate that it is biologically plausible for secondhand-smoke exposure to have cardiovascular effects, such as effects that lead to cardiovascular disease and acute myocardial infarction (MI). The exact mechanisms by which such effects occur, however, remain to be elucidated.

Smoking-Ban Background

Characteristics of smoking bans can heavily influence their consequences. Interpretation of the results of epidemiologic studies that involve smoking bans must account for information on the bans and their enforcement.

Secondhand smoke should have been measured before and after implementation of a ban, and locations with and without bans should have been compared. Studies that include self-reported assessments of exposure to secondhand smoke cannot necessarily be compared with each other unless the survey instruments (such as interviews) were similar.

The comparability of the time and length of followup of the studies should be assessed. For example, the impact of a ban in one area may differ from the impact of a ban in another solely because the observation times were different and other activities may have occurred during the same periods. In comparing studies, it may be impossible to separate contextual factors associated with ban legislation—such as public comment periods, information announcing the ban, and notices about the impending changes—from the impact of the ban itself. The committee therefore included such contextual factors in drawing conclusions about the effects of a ban.

Interpretation needs to consider the timeframes in the epidemiologic evidence, for example, the time from onset of a smoking ban to the mea-

surement of incidence of a disease, the timing and nature of enforcement, and the time until changes in cardiovascular-event rates were observed in people who had various baseline risks. Interpretation should account for the extent to which studies assessed possible alternative causes of decreases in hospitalizations for coronary events, including changes in health-care availability and in the standard of practice in cardiac care, such as new diagnostic criteria for acute MI during the period of study. The latter is especially important in making before–after comparisons in the absence of a comparison geographic area in which no ban has been implemented.

When designing and analyzing future studies, researchers should examine the time between the implementation of a smoking ban and changes in rates of hospital admission or cardiac death. Future studies could evaluate whether decreases in admissions are transitory, sustained, or increasing, and ideally they would include information on individual subjects, including prior history of cardiac disease, to answer the questions posed to the committee.

Epidemiologic Studies

Cardiovascular disease is a major public-health concern. The results of dozens of epidemiologic studies of both case–control and cohort design carried out in multiple populations consistently indicate about a 25–30% increase in risk of coronary heart disease from exposure to secondhand smoke (see Chapter 4 ). Epidemiologic studies using serum cotinine concentration as a biomarker of overall exposure to secondhand smoke indicated that the relative risk (RR) of coronary heart disease associated with secondhand smoke is even greater than those estimates. The excess risk is unlikely to be explained by misclassification bias, uncontrolled-for confounding effects, or publication bias. Although few studies have addressed the risk of coronary heart disease posed by secondhand-smoke exposure in the workplace, there is no biologically plausible reason to suppose that the effect of secondhand-smoke exposure at work or in a public building differs from the effect of exposure in the home environment. Epidemiologic studies demonstrate a dose–response relationship between chronic secondhand-smoke exposure as assessed by self-reports of exposure (He et al., 1999) and as assessed by biomarkers (cotinine) and long-term risk of coronary heart disease (Whincup et al., 2004). Dose–response curves show a steep initial rise in risk when going from negligible to low exposure followed by a gradual increase with increasing exposure.

The INTERHEART study, a large case–control study of cases of first acute MI, showed that exposure to secondhand smoke increased the risk of nonfatal acute MI in a graded manner (Teo et al., 2006).

Eleven key epidemiologic studies evaluated the effects of eight smok-

ing bans on the incidence of acute coronary events (see Table 8-1 and Chapter 6 ). The results of those studies show remarkable consistency: all showed decreases in the rate of acute MIs after the implementation of smoking bans (Barone-Adesi et al., 2006; Bartecchi et al., 2006; CDC, 2009; Cesaroni et al., 2008; Juster et al., 2007; Khuder et al., 2007; Lemstra et al., 2008; Pell et al., 2008; Sargent et al., 2004; Seo and Torabi, 2007; Vasselli et al., 2008). Two of the studies (Pell et al., 2008; Seo and Torabi, 2007) examined rates of hospitalization for acute coronary events after the implementation of smoking bans and provided direct evidence of the relationship of secondhand-smoke exposure to acute coronary events by presenting results in nonsmokers.

The decreases in acute MIs in the 11 studies ranged from about 6 to 47%, depending on characteristics of the study, including the method of statistical analysis. The consistency in the direction of change gave the committee confidence that smoking bans result in a decrease in the rate of acute MI. The studies took advantage of bans as “natural experiments” to look at questions about the effects of bans, and indirectly of a decrease in secondhand-smoke exposure, on the incidence of acute cardiac events. As discussed in Assessing the Health Impact of Air Quality Regulations: Concepts and Methods for Accountability Research (HEI Accountability Working Group, 2003) in the context of air-pollution regulations, studies of interventions constitute a more definitive approach than other epidemiologic studies to determining whether regulations result in health benefits. All the studies are relevant and informative with respect to the questions posed to the committee, and overall they support an association between smoking bans and a decrease in acute cardiovascular events. The studies have inherent limitations related to their nature, but they directly evaluated the effects of an intervention (a smoking ban, including any concomitant activities) on a health outcome of interest (acute coronary events).

The committee could not determine the magnitude of effect with any reasonable degree of certainty on the basis of those studies. The variability in study design, implementation, and analysis was so large that the committee concluded that it could not conduct a meta-analysis or combine the information from the studies to calculate a point estimate of the effect. In particular, the committee was unable to determine the overall portion of the effect attributable to decreased smoking by smokers as opposed to decreased exposure of nonsmokers to secondhand smoke because of a lack of information on smoking status in nine of the studies (Barone-Adesi et al., 2006; Bartecchi et al., 2006; CDC, 2009; Cesaroni et al., 2008; Juster et al., 2007; Khuder et al., 2007; Lemstra et al., 2008; Sargent et al., 2004; Seo and Torabi, 2007; Vasselli et al., 2008). The results of the studies are consistent with the findings of the pathophysiologic studies discussed in Chapter 3 and the data on PM discussed in Chapters 3 and 7 . At the population level,

results of the key intervention studies reviewed by the committee are for the most part consistent with a decrease in risk as early as a month following reductions in secondhand-smoke exposure; however, given the variability in the studies and the lack of data on the precise timing of interventions, the smoking-ban studies do not provide adequate information on the time it takes to see decreases in acute MIs.

Plausibility of Effect

The committee considered both the biologic plausibility of a causal relationship between a decrease in secondhand-smoke exposure and a decrease in the incidence of acute MI and the plausibility of the magnitude of the effect seen in the key epidemiologic studies after implementation of smoking bans.

The experimental data reviewed in Chapter 3 demonstrate that several components of secondhand smoke, as well as secondhand smoke itself, exert substantial cardiovascular toxicity. The toxic effects include the induction of endothelial dysfunction, an increase in thrombosis, increased inflammation, and possible reductions in plaque stability. The data provide evidence that it is biologically plausible for secondhand smoke to be a potential causative trigger of acute coronary events. The risk of acute coronary events is likely to be increased if a person has preexisting heart disease. The association comports with findings on air-pollution components, such as diesel exhaust (Mills et al., 2007) and PM (Bhatnagar, 2006).

As a “reality check” on the potential effects of changes in secondhand-smoke exposure, the committee estimated the decrease in risk of cardiovascular disease and specifically heart failure that would be expected on the basis of the risk effects of changes in airborne PM concentrations after implementation of smoking bans seen in the PM literature. The PM in cigarette smoke is not identical with that in air pollution, and the committee did not attempt to estimate the risk attributable to secondhand-smoke exposure through the PM risk estimates but rather found this a useful exercise to see whether the decreases seen in the epidemiologic literature are reasonable, given data on other air pollutants that have some common characteristics. The committee’s estimates on the basis of the PM literature support the possibility that changes in secondhand-smoke exposure after implementation of a smoking ban can have a substantial effect on hospital admissions for heart failure and cardiovascular disease.

SUMMARY OF OVERALL WEIGHT OF EVIDENCE

The committee examined three relationships—of secondhand-smoke exposure and cardiovascular disease, of secondhand-smoke exposure and

TABLE 8-1 Summary of Key Studies (Studies Listed by Smoking-Ban Region in Order of Publication)

acute coronary events, and of smoking bans and acute coronary events. The committee used the criteria of causation described in Smoking and Health: Report of the Advisory Committee of the Surgeon General of the Public Health Service (U.S. Public Health Service, 1964) in drawing conclusions regarding those relationships. The criteria are often referred to as the Bradford Hill criteria because they were, as stated by Hamill (1997), “later expanded and refined by A. B. Hill” (Hill, 1965). Table 8-2 summarizes the available evidence on secondhand-smoke exposure and coronary events in terms of the Bradford Hill criteria.

Secondhand-Smoke Exposure and Cardiovascular Disease

The results of both case–control and cohort studies carried out in multiple populations consistently indicate exposure to secondhand smoke causes about a 25–30% increase in the risk of coronary heart disease; results of some studies indicate a dose–response relationship. Data from animal studies support the dose–response relationship (see Chapter 3 ). Data from experimental studies of animals and cells and from intentional human-dosing studies indicate that a relationship between secondhand-smoke exposure and coronary heart disease is biologically plausible and consistent with understanding of the pathophysiology of coronary heart disease.

Taking all that evidence together, the committee concurs with the conclusions in the 2006 surgeon general’s report (HHS, 2006) that “the evidence is sufficient to infer a causal relationship between exposure to secondhand smoke and increased risks of coronary heart disease morbidity and mortality among both men and women.” Although the committee found strong and consistent evidence of the existence of a positive association between chronic exposure to secondhand smoke and coronary heart disease, determining the magnitude of the risk (the number of cases that are attributable to secondhand-smoke exposure) proved challenging, and the committee has not done it.

Secondhand-Smoke Exposure and Acute Coronary Events

Two of the epidemiologic studies reviewed by the committee that examine rates of hospitalization for acute coronary events after implementation of smoking bans provide direct evidence related to secondhand smoke exposures. The studies either reported events in nonsmokers only (Monroe, Indiana) (Seo and Torabi, 2007) or analyzed nonsmokers and smokers separately on the basis of serum cotinine concentration (Scotland) (Pell et al., 2008). Both studies showed reductions in the RR of acute coronary events in nonsmokers when secondhand-smoke exposure was decreased after implementation of the bans; this indicates an association between a

decrease in exposure to secondhand smoke and a decrease in risk of acute coronary events. Because of differences between and limitations of the two studies (such as in population, population size, and analysis), they do not provide strong sufficient evidence to determine the magnitude of the decrease in RR.

The effect seen after implementation of smoking bans is consistent with data from the INTERHEART study, a case–control study of 15,152 cases of first acute MI in 262 centers in 52 countries (Teo et al., 2006). Increased exposure to secondhand smoke increased the risk of nonfatal acute MI in a graded manner, with adjusted odds ratios of 1.24 (95% confidence interval [CI], 1.17–1.32) and 1.62 (95% CI, 1.45–1.81) in the least exposed people (1–7 hours of exposure per week) and the most exposed (at least 22 hours of exposure per week), respectively. In contrast, a study using data from the Western New York Health Study collected from 1995 to 2001 found that secondhand smoke was not significantly associated with higher risk of MI (Stranges et al., 2007). That study, however, looked at lifetime cumulative exposure to secondhand smoke, a different exposure metric from that in the other studies and one that does not take into account how recent the exposure is.

The other key epidemiologic studies that looked at smoking bans provide indirect evidence of an association between secondhand-smoke exposure and acute coronary events (Barone-Adesi et al., 2006; Bartecchi et al., 2006; CDC, 2009; Cesaroni et al., 2008; Juster et al., 2007; Khuder et al., 2007; Lemstra et al., 2008; Sargent et al., 2004; Vasselli et al., 2008). Although it is not possible to separate the effect of smoking bans in reducing exposure to secondhand smoke and their effect in reducing active smoking in those studies, because they did not report individual smoking status or secondhand-smoke exposure concentrations, monitoring studies of airborne tracers 1 and biomarkers 2 of exposure to secondhand smoke have demonstrated that exposure to secondhand smoke is dramatically reduced after implementation of smoking bans. Those studies therefore provide indirect evidence that at least part of the decrease in acute coronary events seen after implementation of smoking bans could be mediated by a decrease in exposure to secondhand smoke. It is not possible to determine the differential magnitude of the effect that is attributable to changes in nonsmokers and smokers.

Experimental data show that an association between secondhand-

TABLE 8-2 Evaluation of Available Data in Terms of Bradford-Hill Criteria

smoke exposure and acute coronary events is biologically plausible (see Chapter 3 ). Experimental studies in humans, animals, and cell cultures have demonstrated short-term effects of secondhand smoke as a complex mixture or its components individually (such as oxidants, PM, acrolein, PAHs, benzene, and metals) on the cardiovascular system. There is sufficient evidence from such studies to infer that acute exposure to secondhand smoke at concentrations relevant to population exposures induces endothelial dysfunction, increases inflammation, increases thrombosis, and potentially adversely affects plaque stability. Those effects occur at magnitudes relevant to the pathogenesis of acute coronary events. Furthermore, indirect evidence obtained from studies of ambient PM supports the notion that exposure to PM present in secondhand smoke could trigger acute coronary events or induce arrhythmogenesis in a person with a vulnerable myocardium.

Taking all that evidence together, the committee concludes that there is sufficient evidence of a causal relationship between a decrease in secondhand-smoke exposure and a decrease in the risk of acute MI. Given the variability among studies and their limitations, the committee did not provide a quantitative estimate of the magnitude of the effect.

Smoking Bans and Acute Coronary Events

Nine key studies looked at the overall effect of smoking bans on the incidence of acute coronary events in the overall populations—smokers and nonsmokers—studied (Barone-Adesi et al., 2006; Bartecchi et al., 2006; CDC, 2009; Cesaroni et al., 2008; Juster et al., 2007; Khuder et al., 2007; Lemstra et al., 2008; Sargent et al., 2004; Vasselli et al., 2008). Those studies consistently show a decrease in acute MIs after implementation of smoking bans. The combination of experimental data on secondhand-smoke effects discussed above and exposure data that indicate that secondhand-smoke concentrations decrease substantially after implementation of a smoking ban provides evidence that it is biologically plausible for smoking bans to decrease the rate of acute MIs. The committee concludes that there is an association between smoking bans and a reduction in acute coronary events and, given the temporality and biologic plausibility of the effect, that the evidence is consistent with a causal relationship. Although all the studies demonstrated a positive effect of bans in reducing acute MIs, differences among the studies, including the components of the bans and other interventions that promote smoke-free environments that took place during the bans, limited the committee’s confidence in estimating the overall magnitude of the effect. There is little information on how long it would take for such an effect to be seen inasmuch as the studies have not evaluated periods shorter than a month.

DATA GAPS AND RESEARCH RECOMMENDATIONS

Studies of the effect of indoor smoking bans and secondhand-smoke exposure on acute coronary events should be designed to examine the time between an intervention and changes in the effect and to measure the magnitude of the effect. No time to effect can be postulated for individuals on the basis of the available data, and evaluation of population-based effectiveness of a smoking ban depends on societal actions that implement and enforce the ban and on actions that include smoke reduction in homes, cars, and elsewhere. The decrease in secondhand-smoke exposure does not necessarily occur suddenly—it might decline gradually or by steps. In a likely scenario, once a ban is put into place and enforced, a sharp drop in secondhand-smoke exposure might be seen immediately and followed by a slower decrease in exposure as the population becomes more educated about the health consequences of secondhand smoke and exposure becomes less socially acceptable. Future studies that examine the time from initiation of a ban to observation of an effect and that include followup after initiation of enforcement, taking the social aspects into account, would provide better information on how long it takes to see an effect of a ban. Statistical models should clearly articulate a set of assumptions and include sensitivity analyses. Studies that examine whether decreases in hospital admissions for acute coronary events are transitory or sustained would also be informative.

Many factors are likely to influence the effect of a smoking ban on the incidence and prevalence of acute coronary events in a population. They include age, sex, diet, background risk factors and environmental factors for cardiovascular disease, prevalence of smokers in the community, the underlying rate of heart disease in the community (for example, the rate in Italy versus the United States), and the social environment. Future studies should include direct observations on individuals—including their history of cardiac disease, exposure to other environmental agents, and other risk factors for cardiac events—to assess the impact of those factors on study results. Assessment of smoking status is also needed to distinguish between the effects of secondhand smoke in nonsmokers and the effects of a ban that decreases cigarette consumption or promotes smoking cessation in smokers.

Few constituents of secondhand smoke have been adequately studied for cardiotoxicity. Future research should examine the cardiotoxicity of environmental chemicals, including those in secondhand smoke, to define cardiovascular toxicity end points and establish consistent definitions and measurement standards for cardiotoxicity of environmental contaminants. Specifically, information is lacking on the cardiotoxicity of highly reactive smoke constituents, such as acrolein and other oxidants; on techniques for

quantitating those reactive components; and on the toxicity of low concentrations of benzo[ a ]pyrene, of PAHs other than benzo[a]pyrene, and of mixtures of tobacco-smoke toxicants.

Many questions remain with respect to the pathogenesis of cardiovascular disease and acute coronary events and how secondhand-smoke constituents perturb the pathophysiologic mechanisms and result in disease and death. For example, a better understanding of the factors that promote plaque rupture and how they are influenced by tobacco smoke and PM would provide insight into the mechanisms underlying the cardiovascular effects of secondhand smoke and might lead to better methods of detecting preclinical disease and preventing events.

The committee found only sparse data on the prevalence and incidence of cardiovascular disease and acute coronary events at the national level in general compared with other health end points for which there are central data registries and surveillance of all events, such as the Surveillance, Epidemiology, and End Results (SEER) Program for cancer. Although there are national databases that include acute MI patients—such as the National Registry of Myocardial Infarction (Morrow et al., 2001; Rogers et al., 1994), the Health Care Financing Administration database, and the Cooperative Cardiovascular Project (Ellerbeck et al., 1995)—and the Centers for Disease Control and Prevention’s annual National Hospital Discharge Survey and National Health Interview Survey provide some information on cardiovascular end points, these are not comprehensive or inclusive with respect to hospital participation, patient inclusion, or data capture. A national database that captures all cardiovascular end points would facilitate future epidemiologic studies by allowing the tracking of trends and identification of high-risk populations at a more granular level.

A large prospective cohort study could be very helpful in more accurately estimating the magnitude of the risk of cardiovascular disease and acute coronary events posed by secondhand-smoke exposure. It could be a new study specifically designed to assess effects of secondhand smoke or, as was done with the INTERHEART study, take advantage of existing studies—such as the Framingham Heart Study, the Multi-Ethnic Study of Atherosclerosis, the American Cancer Society’s Cancer Prevention Study-3, the European Prospective Investigation into Cancer and Nutrition study, and the Jackson Heart Study—provided that they have adequate information on individual smoking status and secondhand-smoke exposure (or the ability to measure it, for example, in adequate blood samples). If properly designed, such a study could identify subpopulations at highest risk for acute coronary events from secondhand-smoke exposure in relation to such characteristics as age and sex, and concomitant risk factors, such as obesity.

COMMITTEE RESPONSES TO SPECIFIC QUESTIONS

The committee was tasked with responding to eight specific questions. The questions and the committee’s responses are presented below.

What is the current scientific consensus on the relationship between exposure to secondhand smoke and cardiovascular disease? What is the pathophysiology? What is the strength of the relationship?

On the basis of the available studies of chronic exposure to secondhand smoke and cardiovascular disease, the committee concludes that there is scientific consensus that there is a causal relationship between secondhand-smoke exposure and cardiovascular disease. The results of a number of meta-analyses of the epidemiologic studies showed increases of 25–30% in the risk of cardiovascular disease caused by various exposures. The studies include some that use serum cotinine concentration as a biomarker of exposure and show a dose–response relationship. The pathophysiologic data are consistent with that relationship, as are the data from studies of air pollution and PM. The data in support of the relationship are consistent, but the committee could not calculate a point estimate of the magnitude of the effect (that is, the effect size) given the variable strength of the relationship, differences among studies, poor assessment of secondhand-smoke exposure, and variation in concomitant underlying risk factors.

Is there sufficient evidence to support the plausibility of a causal relation between secondhand smoke exposure and acute coronary events such as acute myocardial infarction and unstable angina? If yes, what is the pathophysiology? And what is the strength of the relationship?

The evidence reviewed by the committee is consistent with a causal relationship between secondhand-smoke exposure and acute coronary events, such as acute MI. It is unknown whether acute exposure, chronic exposure, or a combination of the two underlies the occurrence of acute coronary events, inasmuch as the duration or pattern of exposure in individuals is not known. The evidence includes the results of two key studies that have information on individual smoking status and that showed decreases in risks of acute coronary events in nonsmokers after implementation of a smoking ban. Those studies are supported by information from other smoking-ban studies (although these do not have information on individual smoking status, other exposure-assessment studies have demonstrated that secondhand-smoke exposure decreases after implementation of a smoking ban) and by the large body of literature on PM, especially PM 2.5 , a

constituent of secondhand smoke. The evidence is not yet comprehensive enough to determine a detailed mode of action for the relationship between secondhand-smoke exposure and a variety of intervening and preexisting conditions in predisposing to cardiac events. However, experimental studies have shown effects that are consistent with pathogenic factors in acute coronary events. Although the committee has confidence in the evidence of an association between chronic secondhand-smoke exposure and acute coronary events, the evidence on the magnitude of the association is less convincing, so the committee did not estimate that magnitude (that is, the effect size).

Is it biologically plausible that a relatively brief (e.g., under 1 hour) secondhand smoke exposure incident could precipitate an acute coronary event? If yes, what is known or suspected about how this risk may vary based upon absence or presence (and extent) of preexisting coronary artery disease?

There is no direct evidence that a relatively brief exposure to secondhand smoke can precipitate an acute coronary event; few published studies have addressed that question. The circumstantial evidence of such a relationship, however, is compelling. The strongest evidence comes from airpollution research, especially research on PM. Although the source of the PM can affect its toxicity, particle size in secondhand smoke is comparable with that in air pollution, and research has demonstrated a similarity between cardiovascular effects of PM and of secondhand smoke. Some studies have demonstrated rapid effects of brief secondhand-smoke exposure (for example, on platelet aggregation and endothelial function), but more research is necessary to delineate how secondhand smoke produces cardiovascular effects and the role of underlying preexisting coronary arterial disease in determining susceptibility to the effects. Given the data on PM, especially those from time-series studies, which indicate that a relatively brief exposure can precipitate an acute coronary event, and the fact that PM is a major component of secondhand smoke, the committee concludes that it is biologically plausible for a relatively brief exposure to secondhand smoke to precipitate an acute coronary event.

With respect to how the risk might vary in the presence or absence of preexisting coronary arterial disease, it is generally assumed that acute coronary events are more likely to occur in people who have some level of preexisting disease, although that underlying disease is often subclinical. There are not enough data on the presence of pre-existing coronary arterial disease in the populations studied to assess the extent to which the absence or presence of such preexisting disease affects the cardiovascular risk posed by secondhand-smoke exposure.

What is the strength of the evidence for a causal relationship between indoor smoking bans and decreased risk of acute myocardial infarction?

The key intervention studies that have evaluated the effects of indoor smoking bans consistently have shown a decreased risk of heart attack. Research has also indicated that secondhand-smoke exposure is causally related to heart attacks, that smoking bans decrease secondhand-smoke exposure, and that a relationship between secondhand-smoke exposure and acute coronary events is biologically plausible. All the relevant studies have shown an association in a direction consistent with a causal relationship (although the committee was unable to estimate the magnitude of the association), and the committee therefore concludes that the evidence is sufficient to infer a causal relationship.

What is a reasonable latency period between a decrease in secondhand smoke exposure and a decrease in risk of an acute myocardial infarction for an individual? What is a reasonable latency period between a decrease in population secondhand smoke exposure and a measurable decrease in acute myocardial infarction rates for a population?

No direct information is available on the time between a decrease in secondhand-smoke exposure and a decrease in the risk of a heart attack in an individual. Data on PM, however, have shown effects on the heart within 24 hours, and this supports a period of less than 24 hours. At the population level, results of the key intervention studies reviewed by the committee are for the most part consistent with a decrease in risk as early as a month following reductions in secondhand-smoke exposure; however, given the variability in the studies and the lack of data on the precise timing of interventions, the smoking-ban studies do not provide adequate information on the time it takes to see decreases in heart attacks.

What are the strengths and weaknesses of published population-based studies on the risk of acute myocardial infarction following the institution of comprehensive indoor smoking bans? In light of published studies’ strengths and weaknesses, how much confidence is warranted in reported effect size estimates?

Some of the weaknesses of the published population-based studies of the risk of MI after implementation of smoking bans are

Limitations associated with an open study population and, in some cases, with the use of a small sample.

Concurrent interventions that reduce the observed effect of a smoking ban.

Lack of exposure-assessment criteria and measurements.

Lack of information collected on the time between the cessation of exposure to secondhand smoke and changes in disease rates.

Differences between control and intervention groups.

Nonexperimental design of studies (by necessity).

Lack of assessment of the sensitivity of results to the assumptions made in the statistical analysis.

The different studies had different strengths and weaknesses in relation to the assessment of the effects of smoking bans. For example, the Scottish study had such strengths as prospective design and serum cotinine measurements. The Saskatoon study had the advantage of comprehensive hospital records, and the Monroe County study excluded smokers. The population-based studies of the risk of heart attack after the institution of comprehensive smoking bans were consistent in showing an association between the smoking bans and a decrease in the risk of acute coronary events, and this strengthened the committee’s confidence in the existence of the association. However, because of the weaknesses discussed above and the variability among the studies, the committee has little confidence in the magnitude of the effects and, therefore, thought it inappropriate to attempt to estimate an effect size from such disparate designs and measures.

What factors would be expected to influence the effect size? For example, population age distribution, baseline level of secondhand smoke protection among nonsmokers, and level of secondhand smoke protection provided by the smoke-free law .

A number of factors that vary among the key studies can influence effect size. Although some of the studies found different effects in different age groups, these were not consistently identified. One major factor is the size of the difference in secondhand-smoke exposure before and after implementation of a ban, which would vary and depends on: the magnitude of exposure before the ban, which is influenced by the baseline level of smoking and preexisting smoking bans or restrictions; and the magnitude of exposure after implementation of the ban, which is influenced by the extent of the ban, enforcement of and compliance with the ban, changes in social norms of smoking behaviors, and remaining exposure in areas not covered by the ban (for example, in private vehicles and homes). The baseline rate of acute coronary events or cardiovascular disease could influence the effect

size, as would the prevalence of other risk factors for acute coronary events, such as obesity, diabetes, and age.

What are the most critical research gaps that should be addressed to improve our understanding of the impact of indoor air policies on acute coronary events? What studies should be performed to address these gaps?

The committee identified the following gaps and research needs as those most critical for improving understanding of the effect of indoor-air policies on acute coronary events:

The committee found a relative paucity of data on environmental cardiotoxicity of secondhand smoke compared with other disease end points related to secondhand smoke, such as carcinogenicity and reproductive toxicity. Research should develop standard definitions of cardiotoxic end points in pathophysiologic studies (for example, specific results on standard assays) and a classification system for cardiotoxic agents (similar to the International Agency for Research on Cancer classification of carcinogens). Established cardiotoxicity assays for environmental exposures and consistent definitions of adverse outcomes of such tests would improve investigations of the cardiotoxicity of secondhand smoke and its components and identify potential end points for the investigation of the effects of indoor-air policies on acute coronary events.

The committee found a lack of a system for surveillance of the prevalence of cardiovascular disease and of the incidence of acute coronary events in the United States. Surveillance of incidence and prevalence trends would allow secular trends to be taken into account better and to be compared among different populations to establish the effects of indoor-air policies. Although some national databases and surveys include cardiovascular end points, a national database that tracks hospital admission rates and deaths from acute coronary events, similar to the SEER database for cancer, would improve epidemiologic studies.

The committee found a lack of understanding of a mechanism that leads to plaque rupture and from that to an acute coronary event and of how secondhand smoke affects that process. Additional research is necessary to develop reliable biomarkers of early effects on plaque vulnerability to rupture and to improve the design of pathophysiologic studies of secondhand smoke that examine effects of exposure on plaque stability.

All 11 key studies reviewed by the committee have strengths and limitations due to their study design, and none was designed to test the hypothesis that secondhand-smoke exposure causes cardiovascular disease or acute coronary events. Because of those limitations and the consequent variability in results, the committee did not have enough information to estimate the magnitude of the decrease in cardiovascular risk due to smoking bans or to a decrease in secondhand-smoke exposure. A large, well-designed study could permit estimation of the magnitude of the effect. An ideal study would be prospective; would have individual-level data on smoking status; would account for potential confounders, including other risk factors for cardiovascular events (such as obesity and age), would have biomarkers of mainstream and secondhand-smoke exposures (such as blood cotinine concentrations); and would have enough cases to allow separate analyses of smokers and nonsmokers or, ideally, stratification of cases by cotinine concentrations to examine the dose–response relationship. Such a study could be specifically designed for secondhand smoke or potentially could take advantage of existing cohort studies that might have data available or attainable for investigating secondhand-smoke exposure and its cardiovascular effects, such as was done with the INTERHEART study. Existing studies that could be explored to determine their utility and applicability to questions related to secondhand smoke include the Multi-Ethnic Study of Atherosclerosis (MESA) study, the American Cancer Society’s CPS-3, the European Prospective Investigation of Cancer (EPIC), the Framingham Heart Study, and the Jackson Heart Study. Researchers should clearly articulate the assumptions used in their statistical models and include analysis of the sensitivity of results to model choice and assumptions.

Barone-Adesi, F., L. Vizzini, F. Merletti, and L. Richiardi. 2006. Short-term effects of Italian smoking regulation on rates of hospital admission for acute myocardial infarction. European Heart Journal 27(20):2468-2472.

Bartecchi, C., R. N. Alsever, C. Nevin-Woods, W. M. Thomas, R. O. Estacio, B. B. Bartelson, and M. J. Krantz. 2006. Reduction in the incidence of acute myocardial infarction associated with a citywide smoking ordinance. Circulation 114(14):1490-1496.

Bhatnagar, A. 2006. Environmental cardiology: Studying mechanistic links between pollution and heart disease. Circulation Research 99(7):692-705.

CDC (Centers for Disease Control and Prevention). 2009. Reduced hospitalizations for acute myocardial infarction after implementation of a smoke-free ordinance—city of Pueblo, Colorado, 2002–2006. MMWR—Morbidity & Mortality Weekly Report 57(51):1373-1377.

Cesaroni, G., F. Forastiere, N. Agabiti, P. Valente, P. Zuccaro, and C. A. Perucci. 2008. Effect of the Italian smoking ban on population rates of acute coronary events. Circulation 117(9):1183-1188.

Ellerbeck, E. F., S. F. Jencks, M. J. Radford, T. F. Kresowik, A. S. Craig, J. A. Gold, H. M. Krumholz, and R. A. Vogel. 1995. Quality of care for Medicare patients with acute myocardial infarction. A four-state pilot study from the cooperative cardiovascular project. JAMA 273(19):1509-1514.

Hamill, P. V. 1997. Re: “Invited commentary: Response to Science article, ‘Epidemiology faces its limits.’” American Journal of Epidemiology 146(6):527-528.

He, J., S. Vupputuri, K. Allen, M. R. Prerost, J. Hughes, and P. K. Whelton. 1999. Passive smoking and the risk of coronary heart disease--a meta-analysis of epidemiologic studies. New England Journal of Medicine 340(12):920-926.

HEI (Health Effects Institute) Accountability Working Group. 2003. Assessing the health impact of air quality regulations: Concepts and methods for accountability research. Communication 11. Boston, MA: Health Effects Institute.

HHS (U.S. Department of Health and Human Services). 2006. The health consequences of involuntary exposure to tobacco smoke: A report of the surgeon general. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health.

Hill, A. B. 1965. The environment and disease: Association or causation? Proceedings of the Royal Society of Medicine 58:295-300.

Juster, H. R., B. R. Loomis, T. M. Hinman, M. C. Farrelly, A. Hyland, U. E. Bauer, and G. S. Birkhead. 2007. Declines in hospital admissions for acute myocardial infarction in New York state after implementation of a comprehensive smoking ban. American Journal of Public Health 97(11):2035-2039.

Khuder, S. A., S. Milz, T. Jordan, J. Price, K. Silvestri, and P. Butler. 2007. The impact of a smoking ban on hospital admissions for coronary heart disease. Preventive Medicine 45(1):3-8.

Lemstra, M., C. Neudorf, and J. Opondo. 2008. Implications of a public smoking ban. Canadian Journal of Public Health 99(1):62-65.

Mills, N. L., H. Tornqvist, M. C. Gonzalez, E. Vink, S. D. Robinson, S. Soderberg, N. A. Boon, K. Donaldson, T. Sandstrom, A. Blomberg, and D. E. Newby. 2007. Ischemic and thrombotic effects of dilute diesel-exhaust inhalation in men with coronary heart disease. New England Journal of Medicine 357(11):1075-1082.

Morrow, D. A., E. M. Antman, L. Parsons, J. A. de Lemos, C. P. Cannon, R. P. Giugliano, C. H. McCabe, H. V. Barron, and E. Braunwald. 2001. Application of the TIMI risk score for ST-elevation MI in the National Registry of Myocardial Infarction 3. JAMA 286(11):1356-1359.

Pell, J. P., S. Haw, S. Cobbe, D. E. Newby, A. C. H. Pell, C. Fischbacher, A. McConnachie, S. Pringle, D. Murdoch, F. Dunn, K. Oldroyd, P. Macintyre, B. O’Rourke, and W. Borland. 2008. Smoke-free legislation and hospitalizations for acute coronary syndrome. New England Journal of Medicine 359(5):482-491.

Rogers, W. J., L. J. Bowlby, N. C. Chandra, W. J. French, J. M. Gore, C. T. Lambrew, R. M. Rubison, A. J. Tiefenbrunn, and W. D. Weaver. 1994. Treatment of myocardial infarction in the United States (1990 to 1993). Observations from the National Registry of Myocardial Infarction. Circulation 90(4):2103-2114.

Sargent, R. P., R. M. Shepard, and S. A. Glantz. 2004. Reduced incidence of admissions for myocardial infarction associated with public smoking ban: Before and after study. BMJ 328(7446):977-980.

Seo, D.-C., and M. R. Torabi. 2007. Reduced admissions for acute myocardial infarction associated with a public smoking ban: Matched controlled study. Journal of Drug Education 37(3):217-226.

Stranges, S., M. Cummings, F. P. Cappuccio, and M. Travisan. 2007. Secondhand smoke exposure and cardiovascular disease. Current Cardiovascular Risk Reports 1(5):373-378.

Teo, K. K., S. Ounpuu, S. Hawken, M. R. Pandey, V. Valentin, D. Hunt, R. Diaz, W. Rashed, R. Freeman, L. Jiang, X. Zhang, S. Yusuf, and I. S. Investigators. 2006. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: A case-control study. Lancet 368(9536):647-658.

U.S. Public Health Service. 1964. Smoking and health: Report of the Advisory Committee of the Surgeon General of the Public Health Service . PHS Publication No. 1103. Washington, DC.

Vasselli, S., P. Papini, D. Gaelone, L. Spizzichino, E. De Campora, R. Gnavi, C. Saitto, N. Binkin, and G. Laurendi. 2008. Reduction incidence of myocardial infarction associated with a national legislative ban on smoking. Minerva Cardioangiologica 56(2):197-203.

Whincup, P. H., J. A. Gilg, J. R. Emberson, M. J. Jarvis, C. Feyerabend, A. Bryant, M. Walker, and D. G. Cook. 2004. Passive smoking and risk of coronary heart disease and stroke: Prospective study with cotinine measurement. BMJ 329(7459):200-205.

Data suggest that exposure to secondhand smoke can result in heart disease in nonsmoking adults. Recently, progress has been made in reducing involuntary exposure to secondhand smoke through legislation banning smoking in workplaces, restaurants, and other public places. The effect of legislation to ban smoking and its effects on the cardiovascular health of nonsmoking adults, however, remains a question.

Secondhand Smoke Exposure and Cardiovascular Effects reviews available scientific literature to assess the relationship between secondhand smoke exposure and acute coronary events. The authors, experts in secondhand smoke exposure and toxicology, clinical cardiology, epidemiology, and statistics, find that there is about a 25 to 30 percent increase in the risk of coronary heart disease from exposure to secondhand smoke. Their findings agree with the 2006 Surgeon General's Report conclusion that there are increased risks of coronary heart disease morbidity and mortality among men and women exposed to secondhand smoke. However, the authors note that the evidence for determining the magnitude of the relationship between chronic secondhand smoke exposure and coronary heart disease is not very strong.

Public health professionals will rely upon Secondhand Smoke Exposure and Cardiovascular Effects for its survey of critical epidemiological studies on the effects of smoking bans and evidence of links between secondhand smoke exposure and cardiovascular events, as well as its findings and recommendations.

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Persuasive Essay Guide

Persuasive Essay About Smoking

Persuasive Essay About Smoking - Making a Powerful Argument with Examples

What You Need To Know About Persuasive Essay

A persuasive essay is a type of writing that aims to convince its readers to take a certain stance or action. It often uses logical arguments and evidence to back up its argument in order to persuade readers.

It also utilizes rhetorical techniques such as ethos, pathos, and logos to make the argument more convincing. In other words, persuasive essays use facts and evidence as well as emotion to make their points.

A persuasive essay about smoking would use these techniques to convince its readers about any point about smoking. Check out an example below:

Simple persuasive essay about smoking

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Persuasive Essay Examples About Smoking

Smoking is one of the leading causes of preventable death in the world. It leads to adverse health effects, including lung cancer, heart disease, and damage to the respiratory tract. However, the number of people who smoke cigarettes has been on the rise globally.

A lot has been written on topics related to the effects of smoking. Reading essays about it can help you get an idea of what makes a good persuasive essay.

Here are some sample persuasive essays about smoking that you can use as inspiration for your own writing:

Persuasive speech on smoking outline

Persuasive essay about smoking should be banned

Persuasive essay about smoking pdf

Persuasive essay about smoking cannot relieve stress

Persuasive essay about smoking in public places

Speech about smoking is dangerous

Persuasive Essay About Smoking Introduction

Persuasive Essay About Stop Smoking

Short Persuasive Essay About Smoking

Stop Smoking Persuasive Speech

Check out some more persuasive essay examples on various other topics.

Argumentative Essay About Smoking Examples

An argumentative essay is a type of essay that uses facts and logical arguments to back up a point. It is similar to a persuasive essay but differs in that it utilizes more evidence than emotion.

If you’re looking to write an argumentative essay about smoking, here are some examples to get you started on the arguments of why you should not smoke.

Argumentative essay about smoking pdf

Argumentative essay about smoking in public places

Argumentative essay about smoking introduction

Check out the video below to find useful arguments against smoking:

Tips for Writing a Persuasive Essay About Smoking

You have read some examples of persuasive and argumentative essays about smoking. Now here are some tips that will help you craft a powerful essay on this topic.

Choose a Specific Angle

Select a particular perspective on the issue that you can use to form your argument. When talking about smoking, you can focus on any aspect such as the health risks, economic costs, or environmental impact.

Think about how you want to approach the topic. For instance, you could write about why smoking should be banned.

Check out the list of persuasive essay topics to help you while you are thinking of an angle to choose!

Research the Facts

Before writing your essay, make sure to research the facts about smoking. This will give you reliable information to use in your arguments and evidence for why people should avoid smoking.

You can find and use credible data and information from reputable sources such as government websites, health organizations, and scientific studies.

For instance, you should gather facts about health issues and negative effects of tobacco if arguing against smoking. Moreover, you should use and cite sources carefully.

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Make an Outline

The next step is to create an outline for your essay. This will help you organize your thoughts and make sure that all the points in your essay flow together logically.

Your outline should include the introduction, body paragraphs, and conclusion. This will help ensure that your essay has a clear structure and argument.

Use Persuasive Language

When writing your essay, make sure to use persuasive language such as “it is necessary” or “people must be aware”. This will help you convey your message more effectively and emphasize the importance of your point.

Also, don’t forget to use rhetorical devices such as ethos, pathos, and logos to make your arguments more convincing. That is, you should incorporate emotion, personal experience, and logic into your arguments.

Introduce Opposing Arguments

Another important tip when writing a persuasive essay on smoking is to introduce opposing arguments. It will show that you are aware of the counterarguments and can provide evidence to refute them. This will help you strengthen your argument.

By doing this, your essay will come off as more balanced and objective, making it more convincing.

Finish Strong

Finally, make sure to finish your essay with a powerful conclusion. This will help you leave a lasting impression on your readers and reinforce the main points of your argument. You can end by summarizing the key points or giving some advice to the reader.

A powerful conclusion could either include food for thought or a call to action. So be sure to use persuasive language and make your conclusion strong.

To conclude,

By following these tips, you can write an effective and persuasive essay on smoking. Remember to research the facts, make an outline, and use persuasive language.

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How To Write A Smoking Essay That Will Blow Your Classmates out of the Water

Writing a Smoking Essay. Complete Actionable Guide

A smoking essay might not be your first choice, but it is a common enough topic, whether it is assigned by a professor or left to your choice. Today we’ll take you through the paces of creating a compelling piece, share fresh ideas for writing teen smoking essays, and tackle the specifics of the essential parts of any paper, including an introduction and a conclusion.

Why Choose a Smoking Essay?

If you are free to select any topic, why would you open this can of worms? There are several compelling arguments in favor, such as:

A smoking essay can fit any type of writing assignment. You can craft an argumentative essay about smoking, a persuasive piece, or even a narration about someone’s struggle with quitting. It’s a rare case of a one-size-fits-all topic.
There is an endless number of environmental essay topics ideas . From the reasons and history of smoking to health and economic impact, as well as psychological and physiological factors that make quitting so challenging.
A staggering number of reliable sources are available online. You won’t have to dig deep to find medical or economic research, there are thousands of papers published in peer-reviewed journals, ready and waiting for you to use them.

Essential Considerations for Your Essay on Smoking

Whether you are writing a teenage smoking essay or a study of health-related issues, you need to stay objective and avoid including any judgment into your assignment. Even if you are firmly against smoking, do not let emotions direct your writing. You should also keep your language tolerant and free of offensive remarks or generalizations.

The rule of thumb is to keep your piece academic. It is an essay about smoking cigarettes you have to submit to your professor, not a blog post to share with friends.

How to Generate Endless Smoking Essay Topic Ideas

At first, it might seem that every theme has been covered by countless generations of your predecessors. However, there are ways to add a new spin to the dullest of topics. We’ll share a unique approach to generating new ideas and take the teenage smoking essay as an example. To make it fresh and exciting, you can:

Add a historic twist to your topic. For instance, research the teenage smoking statistics through the years and theorize the factors that influence the numbers.
Compare the data across the globe. You can select the best scale for your paper, comparing smoking rates in the neighboring cities, states, or countries.
Look at the question from an unexpected perspective. For instance, research how the adoption of social media influenced smoking or whether music preferences can be related to this habit.

The latter approach on our list will generate endless ideas for writing teen smoking essays. Select the one that fits your interests or is the easiest to research, depending on the time and effort you are willing to put into essay writing .

How To Write An Essay About Smoking Cigarettes

A smoking essay follows the same rules as an academic paper on any other topic. You start with an introduction, fill the body paragraphs with individual points, and wrap up using a conclusion. The filling of your “essay sandwich” will depend on the topic, but we can tell for sure what your opening and closing paragraphs should be like.

Smoking Essay Introduction

Whether you are working on an argumentative essay about smoking or a persuasive paper, your introduction is nothing but a vessel for a thesis statement. It is the core of your essay, and its absence is the first strike against you. Properly constructed thesis sums up your point of view on the economic research topics and lists the critical points you are about to highlight. If you allude to the opposing views in your thesis statement, the professor is sure to add extra points to your grade.

The first sentence is crucial for your essay, as it sets the tone and makes the first impression. Make it surprising, exciting, powerful with facts, statistics, or vivid images, and it will become a hook to lure the reader in deeper.

Round up the introduction with a transition to your first body passage and the point it will make. Otherwise, your essay might seem disjointed and patchy. Alternatively, you can use the first couple of sentences of the body paragraph as a transition.

Smoking Essay Conclusion

Any argumentative and persuasive essay on smoking must include a short conclusion. In the final passage, return to your thesis statement and repeat it in other words, highlighting the points you have made throughout the body paragraphs. You can also add final thoughts or even a personal opinion at the end to round up your assignment.

Think of the conclusion as a mirror reflection of your introduction. Start with a transition from the last body paragraph, follow it with a retelling of your thesis statement, and complete the passage with a powerful parting thought that will stay with the reader. After all, everyone remembers the first and last points most vividly, and your opening and closing sentences are likely to have a significant influence on the final grade.

Bonus Tips on How to Write a Persuasive Essay About Smoking

With the most challenging parts of the smoking essay out of the way, here are a couple of parting tips to ensure your paper gets the highest grade possible:

Do not rely on samples you find online to guide your writing. You can never tell what grade a random essay about smoking cigarettes received. Unless you use winning submissions from essay competitions, you might copy faulty techniques and data into your paper and get a reduced grade.
Do not forget to include references after the conclusion and cite the sources throughout the paper. Otherwise, you might get accused of academic dishonesty and ruin your academic record. Ask your professor about the appropriate citation style if you are not sure whether you should use APA, MLA, or Chicago.
Do not submit your smoking essay without editing and proofreading first. The best thing you can do is leave the piece alone for a day or two and come back to it with fresh eyes and mind to check for redundancies, illogical argumentation, and irrelevant examples. Professional editing software, such as Grammarly, will help with most typos and glaring errors. Still, it is up to you to go through the paper a couple of times before submission to ensure it is as close to perfection as it can get.
Do not be shy about getting help with writing smoking essays if you are out of time. Professional writers can take over any step of the writing process, from generating ideas to the final round of proofreading. Contact our agents or skip straight to the order form if you need our help to complete this assignment.

We hope our advice and ideas for writing teen smoking essays help you get out of the slump and produce a flawless piece of writing worthy of an A. For extra assistance with choosing the topic, outlining, writing, and editing, reach out to our support managers .

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Smoking cigarettes has historically been a leisurely and highly popular social activity that a litany of people turn to as a way to assuage daily stress, lose weight, and feel socially accepted in a constantly evolving social world. Tobacco, the main ingredient in cigarettes, has high levels of nicotine, which is a highly addictive ingredient that makes it hard for people to quit smoking if nicotine is ingested on a quotidian basis (Woolbright, 1994, p. 337). According to the CDC (2014), cigarette smoking causes over 480,000 deaths annually in the United States alone, which translates into one out of every five people extirpating due to the ingestion of tobacco. A preventable cause of death, cigarette smoking kills more persons than accidents caused due motor vehicle accidents, alcohol consumption, illegal drug use, deaths involving firearms, and the HIV/AIDS virus altogether (Center For Disease Control and Prevention, 2014). Women who smoke tobacco disproportionately suffer from even more health problems as it directly harms not only their reproductive health but also their mortality and morbidity rates of their progeny or future children (American Lung Association, n.d.). People should not smoke because it not only spawns negative health effects but also because it is not economically useful. If people stopped smoking, many lives would be both indirectly and directly saved from premature and preventative deaths as a result.

Doctors and other medical experts pinpoint the various health hazards caused by smoking, especially to the statistics pertaining to the nexus between smoking cigarettes and premature death, in order to convince people to quit smoking. In the past five decades, the risk of premature death in both female and male smokers has profoundly increased (Centers for Disease Control and Prevention, 2014). According to the CDC (2014), smoking cigarettes causes a handful of diseases because it adversely impacts almost all bodily organs and detracts from the general health of enthusiastic smokers. The risk of developing coronary heart disease (COPD), various cardiovascular maladies, and stroke–the leading cause of death in the United States alone–increases two to four times as much due to the damage it spawns to blood vessels because tobacco narrows and thickens them. These ramifications cause rapid heartbeat, which results in higher blood pressure levels which renders smokers vulnerable to blood clots. If blood clots prevent blood from reaching the heart, people put themselves at risk for heart attack due to the fact that the heart does not get enough oxygen and thus kills the heart muscle. In addition, blood clots can also cause a stroke because they can hinder blood flow to the brain. Shockingly, quitting smoking even after just one year drastically enhances an individual’s risk of incurring poor cardiovascular health. Moreover, smoking is directly connected to various respiratory diseases due to the fact that it harms both airways and alveoli, or the minute air vacs, that are in the lungs. Chronic Obstructive Pulmonary Disease (COPD), emphysema, and bronchitis are common forms of lung disease that chronic smokers often develop. In addition, medical experts correlate cigarette smoking with a litany of cancers, which have been pinpointed as the primary cause of lung cancer in individuals who smoke for a protracted period of time. Smoking cigarettes can also spawn various other types of cancer, including cancer in the stomach, liver, kidneys, bladders, pancreas, and oropharynx. Smoking not only puts smokers at risk for these often fatal types of cancer but also to those around smokes as a result of second-hand smoking. Second-hand smoke, according to the CDC (2014), causes an estimated 34,000 deaths per year in non-smokers because they too develop various cardiovascular diseases while an estimated 8,000 persons prematurely dying as a result of stroke (CDC, 2014). They also are put at risk for developing lung cancer by approximately thirty percent, and their risk for heart attack is also amplified. Physicians estimate that if nobody smoked cigarettes around the world, an estimated one out of every three deaths caused by cancer would not manifest (1).

More poignantly, smoking cigarettes negatively impacts women’s reproductive health, and children who are exposed to cigarette smoke suffer from often fatal effects. Many studies have analyzed and outlined the negative ramifications of maternal smoking on both the mother and the baby and/or infant ( Hofhuis, de Jongste, & Merkus, 2003 & Woolbright, 1994). Many states require documentation on birth certificates of maternal tobacco consumption (Woolbright, 1994). Despite the Surgeon General’s stern warning that maternal smoking has been linked to fetal injury, premature birth, and/or low birth rate, 15-37% of pregnant women still smoke cigarettes while pregnant (Hofhuis, de Jongste, & Merkus, 2003). Mothers who smoke also frequently participate in other high-risk behaviors that also negatively impacts the health of their progeny. Additionally, factors including marital and socio-economic status in addition education level affect the outcome of pregnancies due to increased vulnerability to cigarette smoking (Woolbright, 1994, p. 330). Low birth weight is the main impact of maternal smoking, although the existing literature pinpoints infant death and premature birth as major ramifications of it as well. Infant exposure to tobacco after they are born puts him or her at risk of premature death if they develop respiratory diseases in addition to Sudden Infant Death Syndrome (Woolbright, 1994). Hofhuis, de Jongste, and Merkus (2003) assessed how smoking cigarettes during pregnancy in addition to passive smoking thereafter affects both the mortality and morbidity rates in children. Statistics show that other obstetric complications directly linked to smoking, including spontaneous abortions, premature rupture of membranes, ectopic pregnancies, and complications related to the placenta. Smoking also stunts the lung growth that fetuses need in utero, which results in the child suffering from weakened lungs after birth while also exponentially increases the child’s chance of suffering from asthma and a vast array of other crippling respiratory diseases. In addition, it stunts brain development and detracts from the child’s mental acuity.

Health Effects of Cigarette Smoking. (2014, February 6). Centers for Disease Control and Prevention . Retrieved November 21, 2015 from http://www.cdc.gov/tobacco/data_statistics/fact_sheets/health_effects/effects_ cig_smoking/

American Lung Association. (n.d.). Women and tobacco use. American Lung Association . Retrieved November 21, 2015 from http://www.lung.org/stop- smoking/about-smoking/facts- figures/women-and-tobacco-use.html

Ault, R. W., Jr., R. E., Jackson, J. D., Saba, R. S., & Saurman, D. S. (1991). Smoking and Absenteeism. Applied Economics , 23 , 743-754.

Hodgson TA. Cigarette Smoking and Lifetime Medical Expenditures. Millbank Q 1992, 70, 81-125.

Hofhuis, W., de Jongste, J. C., & Merkus, P. J. (2003). Adverse Health Effects of Prenatal and Postnatal Tobacco Smoke Exposure on Children. Arch Dis Child , 88 , 1086-1090.

Woolbright, L. A. (1994). The effects of maternal smoking on infant health. Population Research and Policy Review , 13 (3), 327-339.

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National Center for Chronic Disease Prevention and Health Promotion (US) Office on Smoking and Health. E-Cigarette Use Among Youth and Young Adults: A Report of the Surgeon General [Internet]. Atlanta (GA): Centers for Disease Control and Prevention (US); 2016.

Cover of E-Cigarette Use Among Youth and Young Adults

E-Cigarette Use Among Youth and Young Adults: A Report of the Surgeon General [Internet].

Chapter 1 introduction, conclusions, and historical background relative to e-cigarettes.

Introduction

Although conventional cigarette smoking has declined markedly over the past several decades among youth and young adults in the United States ( U.S. Department of Health and Human Services [USDHHS] 2012 ), there have been substantial increases in the use of emerging tobacco products among these populations in recent years ( Centers for Disease Control and Prevention [CDC] 2015c ). Among these increases has been a dramatic rise in electronic cigarette (e-cigarette) use among youth and young adults. It is crucial that the progress made in reducing cigarette smoking among youth and young adults not be compromised by the initiation and use of e-cigarettes. This Surgeon General’s report focuses on the history, epidemiology, and health effects of e-cigarette use among youth and young adults; the companies involved with marketing and promoting these products; and existing and proposed public health policies regarding the use of these products by youth and young adults.

E-cigarettes include a diverse group of devices that allow users to inhale an aerosol, which typically contains nicotine, flavorings, and other additives. E-cigarettes vary widely in design and appearance, but generally operate in a similar manner and are composed of similar components ( Figure 1.1 ). A key challenge for surveillance of the products and understanding their patterns of use is the diverse and nonstandard nomenclature for the devices ( Alexander et al. 2016 ). These devices are referred to, by the companies themselves, and by consumers, as “e-cigarettes,” “e-cigs,” “cigalikes,” “e-hookahs,” “mods,” “vape pens,” “vapes,” and “tank systems.” In this report, the term “e-cigarette” is used to represent all of the various products in this rapidly diversifying product category. The terms may differ by geographic region or simply by the prevailing preferences among young users. For example, some refer to all cigarette-shaped products as “e-cigarettes” or as “cigalikes,” and some may refer to the pen-style e-cigarettes as “hookah pens” or “vape pens” ( Richtel 2014 ; Lempert et al. 2016 ).

Diversity of e-cigarette products. Source: Photo by Mandie Mills, CDC.

This report focuses on research conducted among youth and young adults because of the implications of e-cigarette use in this population, particularly the potential for future public health problems. Understanding e-cigarette use among young persons is critical because previous research suggests that about 9 in 10 adult smokers first try conventional cigarettes during adolescence ( USDHHS 2012 ). Similarly, youth e-cigarette experimentation and use could also extend into adulthood; however, e-cigarette use in this population has not been examined in previous reports of the Surgeon General. The first Surgeon General’s report on the health consequences of smoking was published in 1964; of the subsequent reports, those published in 1994 and 2012 focused solely on youth and young adults ( USDHHS 1994 , 2012 ). More recently, the 2012 report documented the evidence regarding tobacco use among youth and young adults, concluding that declines in cigarette smoking had slowed and that decreases in the use of smokeless tobacco had stalled. That report also found that the tobacco industry’s advertising and promotional activities are causal to the onset of smoking in youth and young adults and the continuation of such use as adults ( USDHHS 2012 ). However, the 2012 report was prepared before e-cigarettes were as widely promoted and used in the United States as they are now. Therefore, this 2016 report documents the scientific literature on these new products and their marketing, within the context of youth and young adults. This report also looks to the future by examining the potential impact of e-cigarette use among youth and young adults, while also summarizing the research on current use, health consequences, and marketing as it applies to youth and young adults.

Evidence for this report was gathered from studies that included one or more of three age groups. We defined these age groups to be young adolescents (11–13 years of age), adolescents (14–17 years of age), and young adults (18–24 years of age). Some studies refer to the younger groups more generally as youth. Despite important issues related to e-cigarette use in adult populations, clinical and otherwise (e. g ., their potential for use in conventional smoking cessation), that literature will generally not be included in this report unless it also discusses youth and young adults ( Farsalinos and Polosa 2014 ; Franck et al. 2014 ; Grana et al. 2014 ).

Given the recency of the research that pertains to e-cigarettes, compared with the decades of research on cigarette smoking, the “precautionary principle” is used to guide actions to address e-cigarette use among youth and young adults. This principle supports intervention to avoid possible health risks when the potential risks remain uncertain and have been as yet partially undefined ( Bialous and Sarma 2014 ; Saitta et al. 2014 ; Hagopian et al. 2015 ). Still, the report underscores and draws its conclusions from the known health risks of e-cigarette use in this age group.

Organization of the Report

This chapter presents a brief introduction to this report and includes its major conclusions followed by the conclusions of the chapters, the historical background of e-cigarettes, descriptions of the products, a review of the marketing and promotional activities of e-cigarette companies, and the current status of regulations from the U.S. Food and Drug Administration ( FDA ). Chapter 2 (“Patterns of E-Cigarette Use Among U.S. Youth and Young Adults”) describes the epidemiology of e-cigarette use, including current use (i.e., past 30 day); ever use; co-occurrence of using e-cigarettes with other tobacco products, like cigarettes; and psychosocial factors associated with using e-cigarettes, relying on data from the most recent nationally representative studies available at the time this report was prepared. Chapter 3 (“Health Effects of E-Cigarette Use Among U.S. Youth and Young Adults”) documents the evidence related to the health effects of e-cigarette use, including those that are associated with direct aerosol inhalation by users, the indirect health effects of e-cigarette use, other non-aerosol health effects of e-cigarette use, and secondhand exposure to constituents of the aerosol. Chapter 4 (“Activities of the E-Cigarette Companies”) describes e-cigarette companies’ influences on e-cigarette use and considers manufacturing and price; the impact of price on sales and use; the rapid changes in the industry, particularly the e-cigarette companies; and the marketing and promotion of e-cigarettes. Chapter 5 (“E-Cigarette Policy and Practice Implications”) discusses the implications for policy and practice at the national, state, and local levels. The report ends with a Call to Action to stakeholders—including policymakers, public health practitioners and clinicians, researchers, and the public—to work to prevent harms from e-cigarette use and secondhand aerosol exposure among youth and young adults.

Preparation of this Report

This Surgeon General’s report was prepared by the Office on Smoking and Health, National Center for Chronic Disease Prevention and Health Promotion, CDC , which is part of USDHHS . The initial drafts of the chapters were written by 27 experts who were selected for their knowledge of the topics addressed. These contributions are summarized in five chapters that were evaluated by approximately 30 peer reviewers. After peer review, the entire manuscript was sent to more than 20 scientists and other experts, who examined it for its scientific integrity. After each review cycle, the drafts were revised by the report’s scientific editors on the basis of reviewers’ comments. Subsequently, the report was reviewed by various institutes and agencies within USDHHS.

Scientific Basis of the Report

The statements and conclusions throughout this report are documented by the citation of studies published in the scientific literature. Publication lags have prevented an up-to-the-minute inclusion of all recently published articles and data. This overall report primarily cites peer-reviewed journal articles, including reviews that integrate findings from numerous studies and books that were published through December 2015. However, selected studies from 2016 have been added during the review process that provide further support for the conclusions in this report. When a cited study has been accepted for publication, but the publication has not yet occurred because of the delay between acceptance and final publication, the study is referred to as “in press.” This report also refers, on occasion, to unpublished research, such as presentations at a professional meeting, personal communications from a researcher, or information available in various media. These references are employed when acknowledged by the editors and reviewers as being from reliable sources, which add to the emerging literature on a topic.

Major Conclusions
E-cigarettes are a rapidly emerging and diversified product class. These devices typically deliver nicotine, flavorings, and other additives to users via an inhaled aerosol. These devices are referred to by a variety of names, including “e-cigs,” “e-hookahs,” “mods,” “vape pens,” “vapes,” and “tank systems.”
E-cigarette use among youth and young adults has become a public health concern. In 2014, current use of e-cigarettes by young adults 18–24 years of age surpassed that of adults 25 years of age and older.
E-cigarettes are now the most commonly used tobacco product among youth, surpassing conventional cigarettes in 2014. E-cigarette use is strongly associated with the use of other tobacco products among youth and young adults, including combustible tobacco products.
The use of products containing nicotine poses dangers to youth, pregnant women, and fetuses. The use of products containing nicotine in any form among youth, including in e-cigarettes, is unsafe.
E-cigarette aerosol is not harmless. It can contain harmful and potentially harmful constituents, including nicotine. Nicotine exposure during adolescence can cause addiction and can harm the developing adolescent brain.
E-cigarettes are marketed by promoting flavors and using a wide variety of media channels and approaches that have been used in the past for marketing conventional tobacco products to youth and young adults.
Action can be taken at the national, state, local, tribal, and territorial levels to address e-cigarette use among youth and young adults. Actions could include incorporating e-cigarettes into smokefree policies, preventing access to e-cigarettes by youth, price and tax policies, retail licensure, regulation of e-cigarette marketing likely to attract youth, and educational initiatives targeting youth and young adults.
Chapter Conclusions

Chapter 1. Introduction, Conclusions, and Historical Background Relative to E-Cigarettes

E-cigarettes are devices that typically deliver nicotine, flavorings, and other additives to users via an inhaled aerosol. These devices are referred to by a variety of names, including “e-cigs,” “e-hookahs,” “mods,” “vape pens,” “vapes,” and “tank systems.”
E-cigarettes represent an evolution in a long history of tobacco products in the United States, including conventional cigarettes.
In May 2016, the Food and Drug Administration issued the deeming rule, exercising its regulatory authority over e-cigarettes as a tobacco product.

Chapter 2. Patterns of E-Cigarette Use Among U.S. Youth and Young Adults

Among middle and high school students, both ever and past-30-day e-cigarette use have more than tripled since 2011. Among young adults 18–24 years of age, ever e-cigarette use more than doubled from 2013 to 2014 following a period of relative stability from 2011 to 2013.
The most recent data available show that the prevalence of past-30-day use of e-cigarettes is similar among high school students (16% in 2015, 13.4% in 2014) and young adults 18–24 years of age (13.6% in 2013–2014) compared to middle school students (5.3% in 2015, 3.9% in 2014) and adults 25 years of age and older (5.7% in 2013–2014).
Exclusive, past-30-day use of e-cigarettes among 8th-, 10th-, and 12th-grade students (6.8%, 10.4%, and 10.4%, respectively) exceeded exclusive, past-30-day use of conventional cigarettes in 2015 (1.4%, 2.2%, and 5.3%, respectively). In contrast—in 2013–2014 among young adults 18–24 years of age—exclusive, past-30-day use of conventional cigarettes (9.6%) exceeded exclusive, past-30-day use of e-cigarettes (6.1%). For both age groups, dual use of these products is common.
E-cigarette use is strongly associated with the use of other tobacco products among youth and young adults, particularly the use of combustible tobacco products. For example, in 2015, 58.8% of high school students who were current users of combustible tobacco products were also current users of e-cigarettes.
Among youth—older students, Hispanics, and Whites are more likely to use e-cigarettes than younger students and Blacks. Among young adults—males, Hispanics, Whites, and those with lower levels of education are more likely to use e-cigarettes than females, Blacks, and those with higher levels of education.
The most commonly cited reasons for using e-cigarettes among both youth and young adults are curiosity, flavoring/taste, and low perceived harm compared to other tobacco products. The use of e-cigarettes as an aid to quit conventional cigarettes is not reported as a primary reason for use among youth and young adults.
Flavored e-cigarette use among young adult current users (18–24 years of age) exceeds that of older adult current users (25 years of age and older). Moreover, among youth who have ever tried an e-cigarette, a majority used a flavored product the first time they tried an e-cigarette.
E-cigarette products can be used as a delivery system for cannabinoids and potentially for other illicit drugs. More specific surveillance measures are needed to assess the use of drugs other than nicotine in e-cigarettes.

Chapter 3. Health Effects of E-Cigarette Use Among U.S. Youth and Young Adults

Nicotine exposure during adolescence can cause addiction and can harm the developing adolescent brain.
Nicotine can cross the placenta and has known effects on fetal and postnatal development. Therefore, nicotine delivered by e-cigarettes during pregnancy can result in multiple adverse consequences, including sudden infant death syndrome, and could result in altered corpus callosum, deficits in auditory processing, and obesity.
E-cigarettes can expose users to several chemicals, including nicotine, carbonyl compounds, and volatile organic compounds, known to have adverse health effects. The health effects and potentially harmful doses of heated and aerosolized constituents of e-cigarette liquids, including solvents, flavorants, and toxicants, are not completely understood.
E-cigarette aerosol is not harmless “water vapor,” although it generally contains fewer toxicants than combustible tobacco products.
Ingestion of e-cigarette liquids containing nicotine can cause acute toxicity and possibly death if the contents of refill cartridges or bottles containing nicotine are consumed.

Chapter 4. Activities of the E-Cigarette Companies

The e-cigarette market has grown and changed rapidly, with notable increases in total sales of e-cigarette products, types of products, consolidation of companies, marketing expenses, and sales channels.
Prices of e-cigarette products are inversely related to sales volume: as prices have declined, sales have sharply increased.
E-cigarette products are marketed in a wide variety of channels that have broad reach among youth and young adults, including television, point-of-sale, magazines, promotional activities, radio, and the Internet.
Themes in e-cigarette marketing, including sexual content and customer satisfaction, are parallel to themes and techniques that have been found to be appealing to youth and young adults in conventional cigarette advertising and promotion.

Chapter 5. E-Cigarette Policy and Practice Implications

The dynamic nature of the e-cigarette landscape calls for expansion and enhancement of tobacco-related surveillance to include (a) tracking patterns of use in priority populations; (b) monitoring the characteristics of the retail market; (c) examining policies at the national, state, local, tribal, and territorial levels; (d) examining the channels and messaging for marketing e-cigarettes in order to more fully understand the impact future regulations could have; and (e) searching for sentinel health events in youth and young adult e-cigarette users, while longer-term health consequences are tracked.
Strategic, comprehensive research is critical to identify and characterize the potential health risks from e-cigarette use, particularly among youth and young adults.
The adoption of public health strategies that are precautionary to protect youth and young adults from adverse effects related to e-cigarettes is justified.
A broad program of behavioral, communications, and educational research is crucial to assess how youth perceive e-cigarettes and associated marketing messages, and to determine what kinds of tobacco control communication strategies and channels are most effective.
Health professionals represent an important channel for education about e-cigarettes, particularly for youth and young adults.
Diverse actions, modeled after evidence-based tobacco control strategies, can be taken at the state, local, tribal, and territorial levels to address e-cigarette use among youth and young adults, including incorporating e-cigarettes into smoke-free policies; preventing the access of youth to e-cigarettes; price and tax policies; retail licensure; regulation of e-cigarette marketing that is likely to attract youth and young adults, to the extent feasible under the law; and educational initiatives targeting youth and young adults. Among others, research focused on policy, economics, and the e-cigarette industry will aid in the development and implementation of evidence-based strategies and best practices.
Historical Background

Understanding the role of e-cigarettes requires understanding the long history of tobacco use in the United States, including the role of nicotine delivery, the multiple examples of “reduced-harm” products and associated health claims, and the impact of using tobacco products on the public’s health. Since the late nineteenth century, when the “modern” cigarette came into use, scientists and public health officials have linked cigarette smoking to a remarkable number of adverse effects, and it is now recognized as the primary cause of premature death in the United States ( USDHHS 2014 ). Correspondingly, for a century, manufacturers, scientists, entrepreneurs, and public health leaders have promoted or recommended product changes that might remove some of the harmful elements in cigarette smoke. E-cigarettes are among the latest products.

E-cigarettes are designed for users to inhale nicotine, flavorings, and other additives through an aerosol. The claims and marketing strategies employed by the e-cigarette companies, and the efforts made by others to develop scientific and regulatory tools to deal with these new products, both contribute to the current discourse on e-cigarettes. Many lessons for assessing the potential (and future) consequences of these products can be learned from examining the relevant experiences of the past century, especially the introduction of novel products (including e-cigarettes as well as other tobacco and nicotine products) and the claims of reduced exposure to toxins made by the industry and elsewhere.

Early Efforts to Modify Cigarettes

In the 1880s and 1890s, entrepreneurs promoted novel products that allegedly blocked nicotine and other constituents of conventional cigarettes believed to be poisonous. Dr. Scott’s Electric Cigarettes, advertised in Harper’s Weekly, claimed not only to light without matches but also to contain a cotton filter that “strains and eliminates the injurious qualities from the smoke,” including nicotine ( Harper’s Weekly 1887 ). Nicotine delivery was essential to the development of the modern cigarette in the twentieth century; early on, this substance was thought to be addicting and thus vital to retaining customers. In 1913, the Camel brand was a new kind of cigarette that introduced high-nicotine content by using burley tobacco, which was generally too harsh to inhale into the lungs, but was made more inhalable through the addition of casings (e. g ., sugars, licorice) ( Tindall 1992 ; Proctor 2011 ). In 1916, American Tobacco introduced its Lucky Strike blended cigarette, and in 1918 Liggett & Myers ( L &M) reformulated its Chesterfield brand to make it more palatable to users. As the market grew, advertisements for major brands routinely included health-related statements and testimonials from physicians. During the 1930s and 1940s, prominent advertising campaigns included claims like “Not a cough in a carload” (Old Gold) ( Federal Trade Commission [FTC] 1964 , p. LBA-5); “We removed from the tobacco harmful corrosive ACRIDS (pungent irritants) present in cigarettes manufactured in the old-fashioned way” (Lucky Strike) ( FTC 1964 , p. LBA-2); and “Smoking Camels stimulates the natural flow of digestive fluids … increases alkalinity” (Camel) ( FTC 1964 , p. LBA-1a). Thus, early modifications to the cigarette were made so that it was more palatable, had a higher nicotine delivery and uptake, and could be marketed as “safe” ( FTC 1964 ; Calfee 1985 ).

Filters, Tar Reduction, and Light and Low-Tar Cigarettes

The landmark 1964 Surgeon General’s report on smoking and health concluded that cigarette smoking contributed substantially to mortality from certain specific diseases, including lung cancer ( U.S. Department of Health, Education, and Welfare 1964 ). Although the 1964 report considered the topic, it found the evidence insufficient to assess the potential health benefits of cigarette filters. Cigarettes with filters became the norm by the 1960s, and marketing them with an overt message about harm reduction became the standard ( National Cancer Institute [NCI] 1996 ). However, the Surgeon General convened another group of experts on June 1, 1966, to review the evidence on the role played by the tar and nicotine content in health. The group concluded that “[t]he preponderance of scientific evidence strongly suggests that the lower the ‘tar’ and nicotine content of cigarette smoke, the less harmful are the effects” ( Horn 1966 , p. 16,168). Subsequent studies have repeatedly failed to demonstrate health benefits of smoking light and low-tar cigarettes versus full-flavor cigarettes ( Herning et al. 1981 ; Russell et al. 1982 ; Benowitz et al. 1983 , NCI 2001 ).

Over the years, the tobacco industry used multiple methods to reduce the machine-tested yields of tar and nicotine in cigarettes as a way to claim “healthier” cigarettes. Beginning in the 1970s, tobacco companies advertised the tar and nicotine levels for their cigarettes, which encouraged smokers to believe, without substantiation, they could reduce their risk of exposure to these constituents ( Cummings et al. 2002 ; Pollay and Dewhirst 2002 ). In 1996, the FTC issued a statement that it would allow cigarette companies to include statements about tar and nicotine content in their advertising as long as they used a standardized machine-testing method ( Peeler 1996 ).

The Role of Nicotine and Nicotine Delivery

Although the public health community understood early on that nicotine was the primary psycho-active ingredient in cigarette smoke, before the 1980s, little was known about the importance of nicotine in the addiction process beyond what the cigarette manufacturers had learned from their own research. Some scientists warned that due to nicotine addiction, a reduction in nicotine yields, along with decreases in tar, could lead smokers to change their smoking behavior, such as by smoking a greater number of cigarettes to maintain their nicotine intake or changing their behavior in more subtle ways, such as varying the depth of inhalation or smoking more of the cigarette ( Jarvis et al. 2001 ; National Cancer Institute 2001 ; Thun and Burns 2001 ). Not until the 1970s and 1980s, as researchers studying other forms of drug abuse began to apply their research methods to cigarette smoking, did it become apparent that nicotine was similar in its addictive capability to other drugs of abuse, such as heroin and cocaine ( USDHHS 1981 , 1988 ). As described in the 1988 Surgeon General’s report and in subsequent research, symptoms associated with nicotine addiction include craving, withdrawal, and unconscious behaviors to ensure consistent intake of nicotine ( USDHHS 1988 ; al’Absi et al. 2002 ; Hughes 2007 ).

Although the tobacco industry has long understood the importance of nicotine to maintain long-term cigarette smokers through addiction, public health officials did not fully appreciate this in a broad sense until the 1988 Surgeon General’s report, The Health Consequences of Smoking: Nicotine Addiction ( USDHHS 1988 ).

FDA and Nicotine Regulation

In 1988 (and again in 1994), the Coalition on Smoking OR Health and other public-interest organizations petitioned FDA to classify low-tar and nicotine products as drugs and to classify Premier, the short-lived “smokeless cigarette product” from R.J. Reynolds, as an alternative nicotine-delivery system ( Stratton et al. 2001 ). The Coalition on Smoking OR Health cited indirect claims made through advertising and marketing as evidence of R. J. Reynolds’s intent to have the product used for the mitigation or prevention of disease ( Slade and Ballin 1993 ). Meanwhile, FDA launched an investigation into the practices of the tobacco industry, including the manipulation of nicotine delivery. FDA asserted its jurisdiction over cigarettes and smokeless tobacco and issued certain rules governing access to and promotion of these products ( Federal Register 1996 ). On March 21, 2000, the U.S. Supreme Court ruled 5-4 that Congress had not yet given FDA the necessary statutory authority to issue any rules pertaining to tobacco products ( Gottleib 2000 ; FDA v. Brown & Williamson Tobacco Corp. 2000 ). The subsequent debate over control of nicotine products, including their potential impact on youth, ultimately led to the passage of the 2009 Family Smoking Prevention and Tobacco Control Act, which gave FDA authority to regulate tobacco products. Thus, discussions about the introduction of novel nicotine-containing tobacco products in the market during the 1980s and 1990s helped shape the current regulation of tobacco and nicotine products.

New products introduced in the 1990s or later included modified tobacco cigarettes (e. g ., Advance, Omni); cigarette-like products, also called cigalikes (e.g., Eclipse, Accord); and smokeless tobacco products (e.g., Ariva, Exalt, Revel, snus). Advance, made by Brown and Williamson, was test-marketed with the slogan “All of the taste … Less of the toxins.” Vector launched a national advertising campaign for its Omni cigarette with the slogan “Reduced carcinogens. Premium taste.” In addition to the question of whether the claims were supported by sufficient evidence, scientists and tobacco control leaders raised concerns about the potential for adverse consequences associated with novel nicotine and tobacco products marketed for harm reduction, such as a reduction in cessation rates or increased experimentation by children ( Warner and Martin 2003 ; Joseph et al. 2004 ; Caraballo et al. 2006 ). Studies have shown that smokers are interested in trying novel “reduced-exposure” products and perceive them to have lower health risks, even when advertising messages do not make explicit health claims ( Hamilton et al. 2004 ; O’Connor et al. 2005 ; Caraballo et al. 2006 ; Choi et al. 2012 ; Pearson et al. 2012 ).

At FDA ’s request, the Institute of Medicine ( IOM [now the National Academy of Medicine]) convened a committee of experts to formulate scientific methods and standards by which potentially reduced-exposure products (PREPs), whether the purported reduction was pharmaceutical or tobacco related, could be assessed. The committee concluded that “[f]or many diseases attributable to tobacco use, reducing risk of disease by reducing exposure to tobacco toxicants is feasible” ( Stratton et al. 2001 , p. 232). However, it also cautioned that “PREPs have not yet been evaluated comprehensively enough (including for a sufficient time) to provide a scientific basis for concluding that they are associated with a reduced risk of dis ease compared to conventional tobacco use” ( Stratton et al. 2001 , p. 232). The committee added that “the major concern for public health is that tobacco users who might otherwise quit will use PREPs instead, or others may initiate smoking, feeling that PREPs are safe. That will lead to less harm reduction for a population (as well as less risk reduction for that individual) than would occur without the PREP , and possibly to an adverse effect on the population” ( Stratton et al. 2001 , p. 235). Subsequently, in 2006, Judge Kessler cited these findings in her decision which demanded the removal of light and low-tar labeling due to the misleading nature of these claims ( United States v. Philip Morris 2006 ).

The E-Cigarette

Invention of the E-Cigarette

An early approximation of the current e-cigarette appeared in a U.S. patent application submitted in 1963 by Herbert A. Gilbert and was patented in August 1965 (U.S. Patent No. 3,200,819) ( Gilbert 1965 ). The application was for a “smokeless nontobacco cigarette,” with the aim of providing “a safe and harmless means for and method of smoking” by replacing burning tobacco and paper with heated, moist, flavored air. A battery-powered heating element would heat the flavor elements without combustion ( Gilbert 1965 ). The Favor cigarette, introduced in 1986, was another early noncombustible product promoted as an alternative nicotine-containing tobacco product ( United Press International 1986 ; Ling and Glantz 2005 ).

The first device in the recent innovation in e-cigarettes was developed in 2003 by the Chinese pharmacist Hon Lik, a former deputy director of the Institute of Chinese Medicine in Liaoning Province. Lik’s patent application described a kind of electronic atomizing cigarette ( Hon 2013 ). With support from Chinese investors, in 2004 the product was introduced on the Chinese market under the company name Ruyan ( Sanford and Goebel 2014 ). The product gained some attention among Chinese smokers early on as a potential cessation device or an alternative cigarette product.

The e-cigarette was part of the U.S. market by the mid-2000s, and by 2010 additional brands started to appear in the nation’s marketplace, including Ruyan and Janty ( Regan et al. 2013 ). Ruyan gained a U.S. patent for its product with the application stating that the product is “an electronic atomization cigarette that functions as substitutes (sic) for quitting smoking and cigarette substitutes.” (U.S. Patent No. 8,490,628 B2, 2013). In August 2013, Imperial Tobacco Group purchased the intellectual property behind the Ruyan e-cigarette for $75 million. As of 2014 an estimated 90% of the world’s production of e-cigarette technology and products came from mainland China, mainly Guangdong Province and Zhejiang Province ( Barboza 2014 ).

Sales of e-cigarettes in the United States have risen rapidly since 2007. Widespread advertising via television commercials and through print advertisements for popular brands, often featuring celebrities, has contributed to a large increase in e-cigarette use by both adults and youth since 2010 ( Felberbaum 2013 ; King et al. 2013 ; Regan et al. 2013 ). Additionally, marketing through social media, as well as other forms of Internet marketing, has been employed to market these devices ( Huang et al. 2014 ; Kim et al. 2014 ).

In 2013, an estimated 13.1 million middle school and high school students were aware of e-cigarettes ( Wang et al. 2014 ). According to data from the National Youth Tobacco Survey, in 2011 the prevalence of current e-cigarette use (defined as use during at least 1 day in the past 30 days) among high school students was 1.5%; prevalence increased dramatically, however, to 16% by 2015, surpassing the rate of conventional-cigarette use among high school students ( CDC 2016b ; see Chapter 2 ). This equates to 2.4 million high school students and 620,000 middle school students having used an e-cigarette at least one time in the past 30 days in 2015 ( CDC 2016b ).

These trends have led to substantial concern and discussion within public health communities, including state and national public health agencies, professional organizations, and school administrators and teachers. A primary concern is the potential for nicotine addiction among nonsmokers, especially youth and young adults, and that this exposure to nicotine among youth and young adults is harmful. The diversity and novelty of e-cigarette products on the market and ongoing product innovations make assessments of the biological effects of current e-cigarettes under actual conditions of use—such as their long-term harmfulness—difficult to measure. Unanswered questions remain about the risk profile of these devices, their potential use by young people as a first step to other nicotine products, and their total impact on public health. There are diverging opinions about the potential public health impact of these new products. Some public health scientists have highlighted the potential for alternative nicotine products to serve as a substitute for conventional cigarettes and thus a harm reduction tool ( Henningfield et al. 2003 ; Abrams 2014 ). Others have cautioned that the use of alternative nicotine products might become a bridge that may lead to greater tobacco product use—including dual- or multiple-product use—or initiate nicotine addiction among nonsmokers, especially youth ( Cobb et al. 2010 ; Wagener et al. 2012 ; Benowitz and Goniewicz 2013 ; Britton 2013 ; Chapman 2013 ; Etter 2013 ; USDHHS 2014 ). Current evidence is insufficient to reject either of these hypotheses.

E-Cigarette Products

Components and devices.

E-cigarette devices are composed of a battery, a reservoir for holding a solution that typically contains nicotine, a heating element or an atomizer, and a mouthpiece through which the user puffs ( Figure 1.2 ). The device heats a liquid solution (often called e-liquid or e-juice) into an aerosol that is inhaled by the user. E-liquid typically uses propylene glycol and/or glycerin as a solvent for the nicotine and flavoring chemicals

Parts of an e-cigarette device. Source: Photo by Mandie Mills, CDC.

Flavors and E-Cigarettes

The e-liquids in e-cigarettes are most often flavored; a study estimated that 7,700 unique flavors exist ( Zhu et al. 2014 ) and that most of them are fruit or candy flavors ( Figure 1.3 ). A content analysis of the products available via online retail websites documented that tobacco, mint, coffee, and fruit flavors were most common, followed by candy (e. g ., bubble gum), unique flavors (e.g., Belgian waffle), and alcoholic drink flavors (e.g., strawberry daiquiri) ( Grana and Ling 2014 ). Some retail stores are also manufacturers that create custom flavors, which increases the variety of flavors available.

Examples of e-liquid flavors. Source: Photo by Mandie Mills, CDC.

The widespread availability and popularity of flavored e-cigarettes is a key concern regarding the potential public health implications of the products. The concern, among youth, is that the availability of e-cigarettes with sweet flavors will facilitate nicotine addiction and simulated smoking behavior—which will lead to the use of conventional tobacco products ( Kong et al. 2015 ; Krishnan-Sarin et al. 2015 ). Flavors have been used for decades to attract youth to tobacco products and to mask the flavor and harshness of tobacco ( USDHHS 2012 ). Industry documents show that tobacco companies marketed flavored little cigars and cigarillos to youth and to African Americans to facilitate their uptake of cigarettes ( Kostygina et al. 2014 ). Companies also intended flavored smokeless tobacco products to facilitate “graduation” to unflavored products that more easily deliver more nicotine to the user ( USDHHS 2012 ). Various studies have shown that youth are more likely than adults to choose flavored cigarettes and cigars ( CDC 2015b ). Concern over these findings led Congress to include a ban on characterizing flavors for cigarettes, other than tobacco or menthol, in the Tobacco Control Act. A similar concern exists about e-cigarettes, and this concern is supported by studies indicating that youth and young adults who have ever used e-cigarettes begin their use with sweet flavors rather than tobacco flavors ( Kong et al. 2015 ; Krishnan-Sarin et al. 2015 ). Notably, 81.5% of current youth e-cigarette users said they used e-cigarettes “because they come in flavors I like” ( Ambrose et al. 2015 ).

E-Cigarette Devices

First-generation e-cigarettes were often similar in size and shape to conventional cigarettes, with a design that also simulated a traditional cigarette in terms of the colors used (e. g ., a white body with tan mouthpiece). These devices were often called cigalikes, but there were other products designed to simulate a cigar or pipe. Other cigalikes were slightly longer or narrower than a cigarette; they may combine white with tan or may be black or colored brightly. These newer models use a cartridge design for the part of the device that holds the e-liquid, which is either prefilled with the liquid or empty and ready to be filled. The user then squeezes drops of the e-liquid onto a wick (or bit of cotton or polyfil) connected to the heating element and atomizer ( Figure 1.4 ). As e-cigarettes have become more popular, their designs have become more diverse, as have the types of venues where they are sold ( Noel et al. 2011 ; Zhu et al. 2014 ).

E-liquids being poured into an e-cigarette device. Source: Photo by Mandie Mills, CDC.

Second-generation devices include products that are shaped like pens, are comparatively larger and cylindrical, and are often referred to as “tank systems” in a nod to the transparent reservoir that holds larger amounts of e-liquid than previous cartridge-containing models. Third- and fourth-generation devices represent a diverse set of products and, aesthetically, constitute the greatest departure from the traditional cigarette shape, as many are square or rectangular and feature customizable and rebuildable atomizers and batteries. In addition, since the beginning of the availability of e-cigarettes and their component parts, users have been modifying the devices or building their own devices, which are often referred to as “mods.” The differences in design and engineering of the products are key factors in the size, distribution, and amount of aerosol particles and the variability in levels of chemicals and nicotine present in the e-liquid/aerosol and delivered to the user ( Brown and Cheng 2014 ).

E-Cigarette Product Components and Risks

One of the primary features of the more recent generation of devices is that they contain larger batteries and are capable of heating the liquid to a higher temperature, potentially releasing more nicotine, forming additional toxicants, and creating larger clouds of particulate matter ( Bhatnagar et al. 2014 ; Kosmider et al. 2014 ). For instance, one study demonstrated that, at high temperatures (150°C), exceedingly high levels of formaldehyde—a carcinogen (found to be 10 times higher than at ambient temperatures)—are present that are formed through the heating of the e-liquid solvents (propylene glycol and glycerin), although the level of tolerance of actual users to the taste of the aerosol heated to this temperature is debated ( Kosmider et al. 2014 ; CDC 2015a ; Flavor and Extract Manufacturers Association of the United States 2015 ; Pankow et al. 2015 ). There is also concern regarding the safety of inhaling e-cigarette flavorings. Although some manufacturers have claimed their flavorants are generally recognized as safe for food additives (i.e., to be used in preparing foods for eating), little is known about the long-term health effects of inhaling these substances into the lungs ( CDC 2015a ).

Many devices can be readily customized by their users, which is also leading to the concern that these devices are often being used to deliver drugs other than nicotine ( Brown and Cheng 2014 ). Most commonly reported in the news media, on blogs, and by user anecdote is the use of certain types of e-cigarette-related products for delivering different forms of marijuana ( Morean et al. 2015 ; Schauer et al. 2016 ). The tank systems, for example, have been used with liquid tetrahydrocannabinol ( THC ) or hash oil. Some personal vaporizer devices can be used with marijuana plant material or a concentrated resin form of marijuana called “wax.” One study describes the use, in Europe, of e-cigarette devices to smoke marijuana ( Etter 2015 ).

The various e-cigarette products, viewed as a group, lack standardization in terms of design, capacity for safely holding e-liquid, packaging of the e-liquid, and features designed to minimize hazards with use ( Yang et al. 2014 ). All of these design features may have implications for the health impact of e-cigarette use. Notably, from 2010 to 2014, calls to poison control centers in the United States about exposures related to e-cigarettes increased dramatically. According to the American Association of Poison Control Centers (2015) , 271 cases were reported in 2011, but 3,783 calls were reported in 2014. Among all calls, 51% involved exposure among children younger than 5 years of age ( CDC 2014 ). Most poisonings appear to have been caused by exposure to nicotine-containing liquid ( CDC 2014 ). The lack of a requirement for child-resistant packaging for e-liquid containers may have contributed to these poisonings. Since these data were released, one death in the United States has been confirmed in a child who drank e-liquid containing nicotine ( Mohney 2014 ). Additionally, serious adverse reactions, including at least two deaths, have been reported to FDA in cases that could be attributed to the use of e-cigarettes ( FDA 2013 ). This increase in poisonings prompted the Child Nicotine Poisoning Prevention Act of 2015 (2016) , which was enacted in January 2016. This law requires any container of liquid nicotine that is sold, manufactured, distributed, or imported into the United States to be placed in packaging that is difficult to open by children under 5 years of age.

Secondary risks are also of concern regarding e-cigarettes, including passive exposure to nicotine and other chemicals, and adverse events due to device malfunction. Nicotine is a neuroteratogen, and its use by pregnant women exposes a developing fetus to risks that are well documented in the 50th-anniversary Surgeon General’s report on smoking ( USDHHS 2014 ) and include impaired brain development ( England et al. 2015 ) and other serious consequences. Finally, another consequence of the lack of device regulation is the occurrence of battery failures and subsequent explosions. Explosions have typically occurred during charging, resulting in house and car fires, and sometimes causing injuries to those involved. From 2009 to late 2014, 25 incidents of explosions and fires involving e-cigarettes occurred in the United States ( Chen 2013 ; U.S. Fire Administration 2014 ; FDA 2013 ).

E-Cigarette Companies

E-cigarette companies include manufacturers, wholesalers, importers, retailers, distributors, and some other groups that overlap with these entities ( Barboza 2014 ; Whelan 2015 ). Currently, most of the products are manufactured in Shenzhen, Guangdong Province, China ( Cobb et al. 2010 ; Grana et al. 2014 ; Zhu et al. 2014 ). One study placed the number of brands at 466 in January 2014 and found a net increase of 10.5 brands per month ( Zhu et al. 2014 ). All the major tobacco companies (e. g ., Reynolds American, Altria; Table 1.1 ) and many smaller, independent companies are now in the business. When e-cigarettes first entered the U.S. market, they were sold primarily by independent companies via the Internet and in shopping malls at kiosks where those interested could sample the products. A unique feature of the e-cigarette industry, compared to other tobacco and nicotine products, is the recruitment of visitors to their websites as “affiliates” or distributors to help market the products and, in turn, receive commissions on sales ( Grana and Ling 2014 ; Cobb et al. 2015 ). For example, some companies offer a way for users to earn a commission by advertising the products (e.g., a banner ad is placed on one’s website, and when someone clicks on the link and subsequently purchases a product, the website owner gets a percentage commission). Some companies also offer rewards programs for recruiting new customers or for brand loyalty, with web-site users earning points for free or reduced-price products ( Richardson et al. 2015 ).

Multinational tobacco companies with e-cigarette brands.

E-cigarettes are now in widespread national distribution through convenience stores, tobacco stores, pharmacies, “big box” retail chains such as Costco, online retailers, and shops devoted to e-cigarette products (often called “vape shops”) ( Giovenco et al. 2015 ; Public Health Law Center 2015 ). The “vape shops” offer a place to buy customizable devices and e-liquid solutions in many flavors and sometimes include a café or other elements that promote socializing, essentially making such places like a lounge. With the rapid increase in distribution and marketing in the industry, sales have increased rapidly and were projected to reach $2.5 billion in 2014 and $3.5 billion in 2015, including projections for retail and online channels, as well as “vape shops” ( Wells Fargo Securities 2015 ).

The advertising and marketing of e-cigarette products has engendered skepticism among public health professionals and legislators, who have noted many similarities to the advertising claims and promotional tactics used for decades by the tobacco industry to sell conventional tobacco products ( Campaign for Tobacco-Free Kids 2013 ; CDC 2016a ). Indeed, several of the e-cigarette marketing themes have been reprised from the most memorable cigarette advertising, including those focused on freedom, rebellion, and glamor ( Grana and Ling 2014 ). E-cigarette products are marketed with a variety of unsubstantiated health and cessation messages, with some websites featuring videos of endorsements by physicians (another reprisal of old tobacco industry advertising) ( Grana and Ling 2014 ; Zhu et al. 2014 ). Unlike conventional cigarettes, for which advertising has been prohibited from radio and television since 1971, e-cigarette products are advertised on both radio and television, with many ads featuring celebrities. E-cigarettes also are promoted through sports and music festival sponsorships, in contrast to conventional cigarettes and smokeless tobacco products, which have been prohibited from such sponsorships since the Master Settlement Agreement in 1998. E-cigarettes also appear as product placements in television shows and movies ( Grana et al. 2011 ; Grana and Ling 2014 ).

Another key avenue for e-cigarette promotion is social media, such as Twitter, Facebook, YouTube, and Instagram. As is true in the tobacco industry, the e-cigarette industry organizes users through advocacy groups ( Noel et al. 2011 ; Harris et al. 2014 ; Saitta et al. 2014 ; Caponnetto et al. 2015 ). The extensive marketing and advocacy through various channels broadens exposure to e-cigarette marketing messages and products; such activity may encourage nonsmokers, particularly youth and young adults, to perceive e-cigarette use as socially normative. The plethora of unregulated advertising is of particular concern, as exposure to advertising for tobacco products among youth is associated with cigarette smoking in a dose-response fashion ( USDHHS 2012 ).

Federal Regulation of E-Cigarettes

A “Two-Pronged” Approach to Comprehensive Tobacco Control

Since the passage of the Tobacco Control Act in 2009, FDA has had the authority to regulate the manufacturing, distribution, and marketing of tobacco products sold in the United States. FDA had immediate jurisdiction over cigarettes, roll-your-own cigarette tobacco, and smokeless tobacco. In May 2016, FDA asserted jurisdiction over products that meet the statutory definition of a tobacco product, including e-cigarettes, except accessories of these products ( Federal Register 2016 ). That regulation is currently under litigation.

The IOM ’s 2007 report, Ending the Tobacco Problem: A Blueprint for the Nation, established a “two-pronged” strategy for comprehensive tobacco control: (1) full implementation of proven, traditional tobacco control measures such as clean indoor air laws, taxation, and countermarketing campaigns; and (2) “strong federal regulation of tobacco products and their marketing and distribution” ( Bonnie et al. 2007 , p. 1).

Included in FDA ’s broad authority are the restriction of marketing and sales to youth, requiring disclosure of ingredients and harmful and potentially harmful constituents, setting product standards (e. g ., requiring the reduction or elimination of ingredients or constituents), requiring premarket approval of new tobacco products and review of modified-risk tobacco products, and requiring health warnings. The standard for FDA to use many of its regulatory authorities is whether such an action is appropriate for the protection of public health ( Federal Food, Drug, and Cosmetic Act , § 907(a)(3)(A)). The public health standard in the Tobacco Control Act also requires FDA to consider the health impact of certain regulatory actions at both the individual and population levels, including their impact on nonusers, and on initiation and cessation ( Federal Food, Drug, and Cosmetic Act , § 907(a)(3)(B)).

Importantly, the Tobacco Control Act preserves the authority of state, local, tribal, and territorial governments to enact any policy “in addition to, or more stringent than” requirements established under the Tobacco Control Act “relating to or prohibiting the sale, distribution, possession, exposure to, access to, advertising and promotion of, or use of tobacco products by individuals of any age” ( Federal Food, Drug, and Cosmetic Act , § 916(a)(1)). This preservation of state and local authority ensures the continuation of more local-level, comprehensive tobacco control. However, the statute expressly preempts states and localities from establishing or continuing requirements that are different from or in addition to FDA requirements regarding standards for tobacco products, premarket review, adulteration, misbranding, labeling, registration, good manufacturing practices, or modified-risk tobacco products ( Federal Food, Drug, and Cosmetic Act , § 916(a)(2)(A)). But this express preemption provision does not apply to state and local authority to impose requirements relating to the “sale, distribution, possession, information reporting to the State, exposure to, access to, the advertising and promotion of, or use of, tobacco products by individuals of any age …” ( Federal Food, Drug, and Cosmetic Act , § 916(a)(2)(b)). The interaction of these complex provisions related to federal preemption of state law has been the subject of challenges by the tobacco industry to state and local laws. Thus far, courts have upheld certain local ordinances restricting the sale of flavored tobacco products ( National Association of Tobacco Outlets, Inc. v. City of Providence 2013 ; U.S. Smokeless Tobacco Manufacturing Co. v. City of New York 2013 ).

Legal Basis for Regulating E-Cigarettes as Tobacco Products

In the United States, e-cigarettes can be regulated either as products marketed for therapeutic purposes or as tobacco products. Since the advent of e-cigarettes in the United States around 2007, manufacturers have had the option to apply to FDA ’s Center for Drug Evaluation and Research ( CDER ) or Center for Devices and Radiological Health (CDRH) for approval to market e-cigarettes for therapeutic purposes; as of August 2016, no e-cigarette manufacturers have received approval through this avenue.

In 2008 and early 2009, FDA detained multiple shipments of e-cigarettes from overseas manufacturers and denied them entry into the United States on the grounds that e-cigarettes were unapproved drug-device combination products ( FDA 2011 ). Sottera, Inc., which now does business as NJOY, challenged that determination ( Smoking Everywhere, Inc. and Sottera, Inc., d/b/a NJOY v. U.S. Food and Drug Administration, et al. 2010 ; Bloomberg Business 2015 ). Between the filing of the lawsuit and a decision on the motion for preliminary injunction, Congress passed the Tobacco Control Act and the President signed it into law. The Tobacco Control Act defines the term “tobacco product,” in part, as any product, including component parts or accessories, “made or derived from tobacco” that is not a “drug,” “device,” or “combination product” as defined by the Federal Food, Drug, and Cosmetic Act (21 U.S.C. 321(rr)) ( Family Smoking Prevention and Tobacco Control Act 2009 , § 101(a)). The District Court subsequently granted a preliminary injunction relying on the Supreme Court’s decision in Brown and Williamson (1996) and the recently enacted Tobacco Control Act. FDA appealed the decision and the U.S. Court of Appeals for the D.C. Circuit held that e-cigarettes and, therefore, other products “made or derived from tobacco” are not drug/device combinations unless they are marketed for therapeutic purposes, but can be regulated by FDA as tobacco products under the Tobacco Control Act ( Sottera, Inc. v. Food & Drug Administration 2010 ).

On September 25, 2015, FDA proposed regulations to describe the circumstances in which a product made or derived from tobacco that is intended for human consumption will be subject to regulation as a drug, device, or a combination product. The comment period for this proposed regulation closed on November 24, 2015.

Most e-cigarettes marketed and sold in the United States today contain nicotine made or derived from tobacco. Although some e-cigarettes claim that they contain nicotine not derived from tobacco, or that they contain no nicotine at all ( Lempert et al. 2016 ), there may be reason to doubt some of these claims. Currently, synthetic nicotine and nicotine derived from genetically modified, nontobacco plants are cost-prohibitive for e-cigarette manufacturers, although technological advances could eventually increase the cost-effectiveness of using nicotine that was not derived from tobacco ( Lempert et al. 2016 ). The health effects of passive exposure to e-cigarettes with no nicotine, as well as their actual use and the extent of exposure to these products, have just begun to be studied ( Hall et al. 2014 ; Marini et al. 2014 ; Schweitzer et al. 2015 ) and some states and localities are taking steps to regulate e-cigarettes that do not contain nicotine or tobacco ( Lempert et al. 2016 ).

Deeming Rule

The Tobacco Control Act added a new chapter to the Federal Food, Drug, and Cosmetic Act , which provides FDA with authority over tobacco products. The new chapter applied immediately to all cigarettes, cigarette tobacco, roll-your-own tobacco, and smokeless tobacco; and the law included “any other tobacco products that the Secretary of Health and Human Services by regulation deems to be subject to this chapter” ( Federal Food, Drug, and Cosmetic Act , §901 (b)). Therefore, to regulate e-cigarettes as tobacco products, FDA was required to undertake a rulemaking process to extend its regulatory authority to include e-cigarettes.

Prohibitions on adulterated and misbranded products;
Required disclosure of existing health information, including lists of ingredients and documents on health effects;
Required registration of manufacturers;
Required disclosure of a list of all tobacco products, including information related to labeling and advertising;
Premarket review of new tobacco products (i.e., those not on the market on February 15, 2007);
Restrictions on products marketed with claims about modified risk.
Minimum age restrictions to prevent sales to minors;
Requirements to include a nicotine warning; and
Prohibitions on vending machine sales, unless in a facility that never admits youth.

Future Regulatory Options

Product standards, including restrictions on flavors;
Restrictions on promotion, marketing, and advertising, and prohibitions on brand-name sponsorship of events;
Minimum package sizes;
Prohibitions on self-service displays;
Child-resistant packaging and the inclusion of health warnings; and
Regulation of nicotine levels in products.

Despite this broad authority, FDA is prohibited from certain regulatory actions, even if those actions may be appropriate for the protection of public health. Specifically, FDA generally cannot restrict tobacco use in public places, levy taxes on tobacco products, prohibit sales by a specific category of retail outlet (e. g ., pharmacies), completely eliminate nicotine in tobacco products, require prescriptions for tobacco products unless it is marketed for therapeutic purposes, or establish a federal minimum age of sale for tobacco products above 18 years of age. Thus, even if FDA fully exercises all of its existing authority over e-cigarettes, regulation will still need to be complemented at the state and local levels, including efforts previously shown to be effective for conventional tobacco products, such as comprehensive smokefree laws at the state and local levels, pricing strategies, raising the minimum age of sales to minors to 21, and high-impact countermarketing campaigns. In the current context of rising rates of use by youth, localities and states can also implement policies and programs that minimize the individual- and population-level harms of e-cigarettes (see Chapter 5 ).

This chapter presents the major conclusions of this Surgeon General’s report and the conclusions of each chapter. E-cigarettes are presented within their historical context, with an overview of the components of these devices and the types of products. In 2016, FDA announced its final rule to regulate e-cigarettes under the Family Smoking Prevention and Tobacco Control Act. The chapter outlines options for the regulation of e-cigarettes, particularly as they relate to youth and young adults, based on successful smoking policies. The need to protect youth and young adults from initiating or continuing the use of nicotine-containing products forms a strong basis for the need to regulate e-cigarettes at the local, state, and national levels in the future.

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Home — Essay Samples — Nursing & Health — Smoking — Should Smoking Be Made Illegal: Argumentative

Should Smoking Be Made Illegal: Argumentative

Categories: Smoking Smoking Ban Tobacco

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Updated: 8 December, 2023

Words: 674 | Page: 1 | 4 min read

Works Cited

Centers for Disease Control and Prevention. (2021). Health Effects of Cigarette Smoking. https://www.cdc.gov/tobacco/data_statistics/fact_sheets/health_effects/effects_cig_smoking/index.htm
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Foulds, J., Ramstrom, L., Burke, M., & Fagerström, K. (2003). Effect of Smokeless Tobacco (Snus) on Smoking and Public Health in Sweden. Tobacco Control, 12(4), 349–359.
Hatsukami, D. K., & Stead, L. F. (2020). Tobacco Use: Prevention, Cessation, and Control. Oxford University Press.
Hu, T.-W., Lee, A. H.-Y., Mao, Z., & Ong, M. (2016). China at the Crossroads: The Economics of Tobacco and Health. World Scientific Publishing.
National Cancer Institute. (2020). Harms of Cigarette Smoking and Health Benefits of Quitting. https://www.cancer.gov/about-cancer/causes-prevention/risk/tobacco/cessation-fact-sheet
Peto, R., Lopez, A. D., Boreham, J., Thun, M., & Heath, C. Jr. (2016). Mortality from Smoking in Developed Countries 1950-2010: Indirect Estimates from National Vital Statistics. Oxford University Press.
Schick, S., & Glantz, S. (2005). Philip Morris Toxicological Experiments with Fresh Sidestream Smoke: More Toxic than Mainstream Smoke. Tobacco Control, 14(6), 396–404.
U.S. Department of Health and Human Services. (2014). The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health.
World Health Organization. (2019). WHO Global Report on Trends in Prevalence of Tobacco Smoking 2000-2025, Second Edition. World Health Organization.

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John Sinclair, 82, Dies; Counterculture Activist Who Led a ‘Guitar Army’

His imprisonment for a minor marijuana offense became a cause célèbre. He was released after John Lennon and Yoko Ono sang about him at a protest rally.

A black-and-white photo of John Sinclair, a young man with long dark hair, a mustache and wire-rimmed glasses. He wears a black jacket and holds up a fist.

By Michael S. Rosenwald

John Sinclair, a counterculture activist whose nearly 10-year prison sentence for sharing joints with an undercover police officer was cut short after John Lennon and Yoko Ono sang about his plight at a protest rally, died on Tuesday in Detroit. He was 82.

His publicist, Matt Lee, said the cause of his death, in a hospital, was congestive heart failure.

As the leader of the White Panther Party in the late 1960s, Mr. Sinclair spoke of assembling a “guitar army” to wage “total assault” on racists, capitalism and the criminalization of marijuana. “We are a whole new people with a whole new vision of the world,” he wrote in his book “Guitar Army” (1972), “a vision which is diametrically opposed to the blind greed and control which have driven our immediate predecessors in Euro-Amerika to try to gobble up the whole planet and turn it into one big supermarket.”

He also managed the incendiary Detroit rock band the MC5. Their lyrics — “I’m sick and tired of paying these dues/And I’m finally getting hip to the American ruse” — were a kind of ballad for the cause.

Mr. Sinclair’s command of this “raggedy horde of holy barbarians,” as he described them in his book, was upended in 1969 when Judge Robert J. Colombo of Detroit Recorder’s Court sentenced him to nine and a half to 10 years in prison for giving two joints to an undercover police officer.

During the hearing, Mr. Sinclair argued that he had been framed.

“Everyone who is taking part in this is guilty of violating the United States Constitution and violating my rights and everyone else that’s concerned,” he said. He added, “There is nothing just about this, there is nothing just about these courts, nothing just about these vultures over here.”

In prison, he was responsible for folding underwear but spent most of his time reading and writing. “This is the best thing that’s ever happened to me or our organization,” he told Big Fat magazine during his incarceration. Asked why, he said, “It exposes the fascists who put me here.”

Mr. Sinclair’s case became a cause célèbre in the counterculture movement. On Dec. 10, 1971, 15,000 supporters attended a rally and concert at Crisler Arena in Ann Arbor, Mich. They brought a lot of marijuana with them.

“People were not only smoking joints openly and passing them around,” Keith Stroup, the founder of the marijuana advocacy group NORML (the National Organization for the Reform of Marijuana Laws), wrote , “but several people, including one sitting near my seat, had quantities of marijuana sitting open on their laps, freely rolling joint after joint, to make sure everyone who attended could get high for the occasion.”

Mr. Sinclair spoke to the audience from prison over a phone line connected to the arena’s speaker system.

“Say something to me,” he said, and the crowd shouted, “Free John!”

Among the musicians who performed were Stevie Wonder and Bob Seger. Allen Ginsberg and Abbie Hoffman spoke, along with Bobby Seale, a founder of the Black Panther Party. The event was supposed to end at midnight, but it kept going, and at around 3 a.m. Mr. Lennon and Ms. Ono appeared onstage. The audience went berserk.

With the antiwar activist Jerry Rubin playing drum in the background, Mr. Lennon and Ms. Ono performed a song they had written for Mr. Sinclair. It began:

It ain’t fair, John Sinclair In the stir for breathin’ air Won’t you care for John Sinclair? In the stir for breathin’ air Let him be, set him free Let him be like you and me.

A few days later, the Michigan Supreme Court announced that it was reviewing the case. Mr. Sinclair was released on bond. The court later overturned the conviction.

Justice John B. Swainson held that Mr. Sinclair had been entrapped by Detroit police officers. Two other justices, Thomas E. Brennan and Paul L. Adams, wrote that Mr. Sinclair’s sentence was “cruel and unusual punishment in light of the case against him.”

“Today is a great victory,” Mr. Sinclair said at a news conference, puffing on a joint.

John Alexander Sinclair Jr. was born on Oct. 2, 1941, in Flint, Mich. His father worked for Buick Motors, first on the assembly line and later in management. His mother, Elsie (Newberry) Sinclair, was a teacher. The family lived in Davison, a small town near Flint.

“I grew up there on Lapeer Street, the last street in town going east, and there were fields and woods out beyond our backyard where all the kids on the block spent a lot of time,” he wrote in “Guitar Army.” “They’ve got subdivisions out there now, of course, but then they’ve got a big ‘marijuana problem’ in Davison now, too, which just goes to show you.”

He graduated from the University of Michigan in 1964 with a bachelor’s degree in American literature. He pursued a master’s degree in English literature at Wayne State University in Detroit, but he was expelled “because I was a dope fiend,” he told The Detroit Free Press.

Mr. Sinclair stayed in the city. He wrote poetry, organized jazz concerts and started an artists’ workshop with his girlfriend, Magdalene Arndt, known as Leni. They married in 1965 and became active in the local counterculture movement. With his friend Pun Plamondon, they started the White Panther Party in 1968.

“We thought,” Mr. Sinclair wrote in “Guitar Army,” “that political organization and political theory were things of the past which had no relevance to the contemporary situation, that whatever happened would have to happen spontaneously if it was going to mean anything at all, and that all we had to do was to keep pumping out our propaganda as hard as we could and then just wait for the right moment to present itself, at which time there would be a huge apocalyptic flash and the future of the world would be settled in a matter of days.”

But in a matter of months, Mr. Sinclair was in prison. While there, he was indicted along with Mr. Plamondon and another White Panther Party member on charges that they had conspired in 1968 to bomb a C.I.A. recruiting office in Ann Arbor. The case against them was built on wiretaps for which the F.B.I. had not obtained warrants, and it collapsed after the U.S. Supreme Court ruled that the wiretaps were unconstitutional .

John and Leni Sinclair divorced in 1978. He married Patricia Brown in 1989. She survives him, along with two daughters from his first marriage, Celia and Sunny Sinclair; three stepdaughters, Krishna Tyson, Chonita Robinson and Kenya Makeba Carr; a sister, Kathleen Sinclair-Smith; and a granddaughter.

After his legal problems ended, Mr. Sinclair settled into a life of advocacy, writing poetry and articles for alternative newspapers and producing music festivals. He smoked marijuana every day. After Michigan legalized it in 2018, Mr. Sinclair was among the first customers in line when it became available for purchase.

“Things have come full circle, haven’t they, John?” someone in line asked him, according to MLive , a Michigan news outlet.

Mr. Sinclair replied, “It would be more full if they came and gave me back the weed that they took.”

On Why One Should Stop Smoking Essay (Speech)

Introduction.

Credibility material: how do you really feel when some of the problems you or your relative or even friends face due to smoking? And is it possible to stop smoking after you have been told that smoking will definitely give you serious health problems? Well, I had a friend who became a chain smoker. He used to wake and the first thing that went into his mouth was a cigarette stick, then any other thing will follow thereafter. My friend had been experiencing persistent coughs that made him suspect he might have contracted HIV virus yet he had not yet spent with a woman. But he went for HIV test which proved negative. He continued smoking as he sought out the cough issue in his own ways. One day he became very ill and the cough became even worse. As a friend I accompanied him to a local hospital where he was diagnosed with cancer. The doctor’s advice was that he should stop smoking; however, he never adhered to the doctor’s advice and later died of serious cancer. That was a sad event caused by what could be avoided.

Link to the audience: one of the people who have suffered health complications or death as a result of smoking may be somebody close to you or someone you know.
Thesis and preview: today I am privileged to have your audience and I intend to talk to you about the effects of smoking, and also I propose to give a talk on how to solve the problem of smoking.

Shift into the main section of the speech: I will begin by telling you how smoking affects us.

So many people around the world have suffered the effects of smoking. I will talk about these effects in terms of health and financial effects.

Research has found out that non-smokers are also exposed to dangers related to smoking. It can lead to increased effects of asthma on those who already have asthma, especially children. Taking for instance, available statistics indicate that in the United States of America alone, 53,000 non-smokers are killed by issues related to smoking (San Francisco Tobacco Free Project para1).
To those who have coronary diseases, second hand smoking increases the risk of the disease and can make it severe. Moreover, those who have high risk factors of the disease can easily be attacked when exposed to smoking environment for long.
Imagine that being exposed to second hand smoke for only thirty minutes is enough to cause damages to your heart and the damages are just similar to those of an actual or habitual smoker.
Smoking also affects the unborn: the fetus is affected by secondary smoke inhaled by the mother.
In women who are young and have not reached menopause, secondary smoke increases the risk of breast cancer.
Other effects are impaired learning ability of children, increased risk of experiencing spinal pain, and reduced median cotinine levels (Bonnie pp.5-21).Transition: I believe that you can now realize that smoking does not only affect the smoker, but even the non-smokers and the unborn. The problems related to smoking affects all of us, but the smokers are more exposed than non-smokers even though in some of the problems both groups suffer are just the same. Now I will tell you about the risks smokers directly face.

Habitual smokers are exposed to:

Habitual smokers are at a very high risk of cancer. It has been known that smoking is one of the leading causes of cancer. Taking the case of United Kingdom alone, approximately 106, 000 individuals die annually due to smoke related cancer.
Some of the diseases caused and or worsened by smoking include, lung cancer, diseases of the heart, chronic obstructive pulmonary diseases and also circulation problems.
To pregnant women, smoking is highly likely to cause miscarriages, complications, poor development of the child which may continue after birth and it may also result into still birth or death of the child in the first one week of birth (Litt 29).
Smoking also has economic and other effects on smokers. Smokers, especially heavy chain smokers, use a lot of money as cigarette expenditures. Some of other effects of smoking include, bad breath, clothes and home environment smell stale tobacco, reduces sense of taste, life insurance of smokers are damn expensive and potential employers may not like smokers due to the possibility of constant seek leave.Transition: you can see how much risk smokers are exposed to. It is important to note that these risks can potentially result into deaths. However, it is possible to avoid all these smoking related problems. Now, my last discussion will be on how to solve the problem of smoking.

The only effective way in solving the problem is to stop smoking. But the question somebody may be asking is, “How do I stop smoking?” I will give some ways on how to do so:

Will power is one of the ways to use in solving the problems but the most difficult of all other ways. One should have the courage and have undying persistence on quitting smoking.
Use nicotine-based chewing gum; even though they still contain nicotine, however, the victim under treatment is not getting the tar into the body system.
Use anti-depressants under a medical doctor’s guide.
It is important to stop smoking once diagnosed with problems related with smoking
Another way to stop smoking is to seek the intervention of a counselor who will guide you on gradual processes of stopping smoking.
Non-smokers, especially with risky diseases, should avoid smoking environments (Acts 50).

Brakelight/intention to stop: as you can realize, stopping smoking and campaigning against it will be beneficial to all of us.

Summary: I have talked to you about the effects of smoking on both habitual smokers and non-smokers and also on how the problems can be stopped or avoided. All of us must rise up and campaign against smokers or else we will gradually be affected and infected.

Link back to the audience: now that you know the effects of smoking and how to solve it will you help somebody stop smoking? How happy will you be or satisfied will you feel if someone is to come to thank you for helping him or her stop smoking? Let us take the challenge.

Concluding remark: I am going to stop here, but not before I give you a quote by somebody known as Dr. Gro Harlem Brundtland. “A cigarette is the only consumer product which when used as directed kills its consumer.”

Acts, Humbler. How to Stop Smoking in 50 Days . New York: Bookway International Services, 2001.

Bonnie, Richard. Ending the Tobacco Problem: A Blueprint for the Nation . New York: National Academies Press, 2007.

Litt, Iris. Taking our pulse: The health of America’s women . New York: Stanford University Press, 1997.

San Francisco Tobacco Free Project. “Untitled.” 2010.

Chicago (A-D)
Chicago (N-B)

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Bibliography

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