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Cigarettes and other forms of tobacco are addicting. Most smokers use tobacco regularly because they are addicted to nicotine. Furthermore, most smokers find it difficult to quit using tobacco because they are addicted to nicotine. Nicotine addiction develops in the first few years of cigarette smoking. that is, for most people during adolescence or early adulthood. Most smokers begin smoking during childhood or adolescence: 89% of daily smokers tried their first cigarette by or at age 18, and 71% of persons who have ever smoked daily began smoking daily by age 18 (table 2-1). The earlier in life a child tries a cigarette the more likely he or she is to become a regular smoker (that is, to smoke monthly or more frequently) or a daily smoker. For example, 67% of children who initiate smoking in the sixth grade become regular adult smokers, and 46% of teenagers who initiate smoking in the eleventh grade become regular adult smokers.1 Furthermore, the earlier a youth begins smoking, the more cigarettes he or she will smoke as an adult.2 Prevention of tobacco addiction and the related health consequences, therefore, requires early intervention for children and adolescents. To understand why youths use tobacco and why prevention measures are necessary and preferable to cessation measures to deter tobacco use by youths, it is useful to understand nicotine dependency. This chapter reviews (1) the general aspects of nicotine dependency, derived from research primarily in adults, and (2) the evidence of nicotine dependency and the factors that promote initiation and progression of tobacco use by youths.

*The terms "drug addiction" and "drug dependency" are used interchangeably in this report, as was done in the 1988 report of the surgeon general on nicotine addiction. which considered the terms to be "scientifically equivalent.''



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Page 29 Cigarettes and other forms of tobacco are addicting. Most smokers use tobacco regularly because they are addicted to nicotine. Furthermore, most smokers find it difficult to quit using tobacco because they are addicted to nicotine. Nicotine addiction develops in the first few years of cigarette smoking. that is, for most people during adolescence or early adulthood. Most smokers begin smoking during childhood or adolescence: 89% of daily smokers tried their first cigarette by or at age 18, and 71% of persons who have ever smoked daily began smoking daily by age 18 (table 2-1). The earlier in life a child tries a cigarette the more likely he or she is to become a regular smoker (that is, to smoke monthly or more frequently) or a daily smoker. For example, 67% of children who initiate smoking in the sixth grade become regular adult smokers, and 46% of teenagers who initiate smoking in the eleventh grade become regular adult smokers.1 Furthermore, the earlier a youth begins smoking, the more cigarettes he or she will smoke as an adult.2 Prevention of tobacco addiction and the related health consequences, therefore, requires early intervention for children and adolescents. To understand why youths use tobacco and why prevention measures are necessary and preferable to cessation measures to deter tobacco use by youths, it is useful to understand nicotine dependency. This chapter reviews (1) the general aspects of nicotine dependency, derived from research primarily in adults, and (2) the evidence of nicotine dependency and the factors that promote initiation and progression of tobacco use by youths. *The terms "drug addiction" and "drug dependency" are used interchangeably in this report, as was done in the 1988 report of the surgeon general on nicotine addiction. which considered the terms to be "scientifically equivalent.''

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Page 30 TABLE 2-1  Cumulative percentages of recalled age at which persons aged 30 39 first tried a cigarette or began smoking daily   All persons (n = 6,388) Persons who had ever tried a cigarette Persons who had ever smoked daily Age (years) First tried a cigarette First tried a cigarette First tried a cigarette Began smoking daily <12 14.1 18.0 15.6 1.9 <14 29.7 38.0 36.7 8.0 <16 48.2 61.9 62.2 24.9 <18 63.7 81.6 81.9 53.0 <18 68.8 88.2 89.0 71.2 <20 71.0 91.0 91.3 77.0 Source: National Household Surveys on Drug Abuse United States 1991. Cited in Centers for Disease Control and Prevention. Preventing Tobacco Use Among Young People. A Report of the Surgeon General. Washington DC: U.S. Government Printing Office 1994. 65. GENERAL ASPECTS OF NICOTINE ADDICTION The Daily Nicotine Addiction Cycle Given the pharmacologic properties of nicotine, a daily cycle of addiction can be described as follows. The first cigarette of the day produces substantial pharmacologic effects (pleasure, arousal, enhanced performance), but simultaneously the brain's chemistry changes and tolerance begins to develop. With subsequent cigarettes, nicotine accumulates in the body and is associated with the development of a greater level of tolerance. Withdrawal symptoms become more pronounced between successive cigarettes. The tolerance that develops over the day may be partially overcome by the transiently high brain levels of nicotine that occur immediately after the smoking of individual cigarettes, but the primary pleasurable effects of individual cigarettes tend to lessen throughout the day. As the day progresses, people tend to smoke more to relieve the symptoms of abstinence. Overnight abstinence allows considerable resensitization to the actions of nicotine, and the cycle begins again the next day. What Is Addiction? The World Health Organization (WHO) describes drug dependence as "a behavioral pattern in which the use of a given psychoactive drug is given a sharply higher priority over other behaviors that once had a significantly higher

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Page 31 value."3 In other words, the drug comes to control behavior to an extent considered detrimental to the individual or to society. Historically, drug addiction meant that tolerance developed to the effects of a drug during repetitive use, and that after cessation of such use withdrawal symptoms emerged (termed physical dependence). The prototypical addictive drug was heroin, and drug addiction has had a connotation of social deviance or criminal behavior in the United States. This historical view of addiction was revised by the 1964 Expert Committee of the World Health Organization. As discussed in detail in the 1988 surgeon general's report, such a definition is narrow and does not address addictions such as cocaine or binge alcoholism. A definition based on concepts of drug dependence developed by expert committees of WHO and in publications of the National Institute on Drug Abuse (NIDA) and the American Psychiatric Association includes compulsive drug-seeking behavior, effect of the drug on the brain, and usually a need for the drug to maintain homeostasis. Specific criteria for a drug that produces dependence or addiction have been presented by the U.S. surgeon general (table 2-2), and specific criteria for diagnosing drug dependence or addiction in individuals have been presented by the American Psychiatric Association (table 2-3). Pharmacologic Aspects of Nicotine The pharmacologic effects of nicotine are essential to sustaining cigarette smoking.4 Viewed another way, tobacco is used by people to deliver nicotine to TABLE 2-2 Criteria for drug dependence Primary criteria      Highly controlled or compulsive use      Psychoactive effects      Drug-reinforced behavior Additional criteria      Addictive behavior often involves the following:           Stereotypic patterns of use           Use despite harmful effects           Relapse following abstinence           Recurrent drug cravings      Dependence-producing drugs often manifest the following:           Tolerance           Physical dependence           Pleasant (euphoric) effects Source: Adapted from Centers for Disease Control. The Health Consequences of Smoking: Nicotine Addiction. A Report of the Surgeon General. DHHS Pub. No. (CDC) 88-8406. Washington, DC: U.S. Department of Health and Human Services, 1988. 7.

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Page 32 TABLE 2-3   Criteria for substance dependence A maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three (or more) of the following, occurring at any time in the same 12-month period: 1. Tolerance, as defined by either of the following:     a. A need for markedly increased amounts of the substance to achieve intoxication or         desired effect.     b. Markedly diminished effect with continued use of the same amount of the         substance. 2. Withdrawal, as manifested by either of the following:     a. The characteristic withdrawal syndrome for the substance (refer to Criteria A and B         of the criteria sets for withdrawal from the specific substance).     b. The same (or a closely related) substance is taken to relieve or avoid withdrawal symptoms. 3. The substance is often taken in larger amounts or over a longer period than was intended. 4. There is a persistent desire or unsuccessful efforts to cut down or control substance use. 5. A great deal of time is spent in activities necessary to obtain the substance (e.g., visiting multiple doctors or driving long distances), use the substance (e.g., chain-smoking), or recover from its effects. 6. Important social, occupational, or recreational activities are given up or reduced because of substance abuse. 7. The substance use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance (e.g., current cocaine use despite recognition of cocaine-induced depression, or continued drinking despite recognition that an ulcer was made worse by alcohol consumption) Source: American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: DSM-IV. 4th ed. Washington, DC: American Psychiatric Association, 1994. 181. the body. The primary physiologic effects of nicotine (reviewed in detail in the 1988 surgeon general's report) are listed below. · Electroencephalographic desynchronization · Increased circulating levels of catecholamines, vasopressin, growth hormone, adrenocorticotropic hormone, cortisol, prolactin, and beta-endorphin · Increased metabolic rate · Lipolysis, increased free fatty acids · Heart rate acceleration

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Page 33 · Cutaneous and coronary vasoconstriction · Increased cardiac output · Increased blood pressure · Skeletal muscle relaxation Smokers give various explanations for their smoking. Many report that smoking produces arousal, particularly with the first few cigarettes of the day, and relaxation, particularly in stressful situations. Many smokers report that smoking helps them concentrate and lifts their mood. Nicotine has been shown to increase vigilance in the performance of repetitive tasks and to enhance selective attention. Smokers commonly report pleasure and reduced anger, tension, depression, and stress after smoking a cigarette. The extent to which the enhanced performance and mood after smoking are due to the relief of symptoms of abstinence or to an intrinsic enhancement effect on the brain is unclear. A few studies do show improvement in the performance of nonsmoking subjects after dosing with nicotine, suggesting at least some direct enhancement. Some of the gratifying effects of nicotine are due to the relief of the symptoms of nicotine withdrawal. When nicotine use is abruptly stopped, withdrawal symptoms emerge. The typical symptoms are listed below. · Restlessness · Eating more than usual · Anxiety/tension · Impatience · Irritability/anger · Difficulty concentrating · Excessive hunger · Depression · Disorientation · Loss of energy/fatigue · Dizziness · Stomach or bowel problems · Headaches · Sweating · Insomnia · Heart palpitations · Tremors · Craving cigarettes5 Most withdrawal symptoms reach maximal intensity 24 to 48 hours after cessation of tobacco use and gradually diminish in intensity over several weeks. Some symptoms, such as eating more than usual, weight gain, and craving cigarettes (particularly in stressful situations) may persist for months or even years after cessation.

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Page 34 Actions of Nicotine on the Brain The nicotine molecule is shaped like acetylcholine. Acetylcholine is a neurotransmitter, that is, a chemical naturally found in the body that is involved in transmitting information from one neuron to another. Receptors (specialized proteins that selectively bind drugs and initiate drug effects in the body) for acetylcholine are called cholinergic receptors. Nicotine acts on certain cholinergic receptors in the brain and other organs of the body. The receptors would normally be acted on by the body's own acetylcholine. By activating cholinergic receptors, nicotine enhances the release of other neurotransmitters and hormones including acetylcholine, norepinephrine, dopamine, vasopressin, serotonin, and beta-endorphin. The physiologic effects of nicotine include behavioral arousal and sympathetic neural activation. Release of specific neurotransmitters has been speculatively linked to particular reinforcing effects of nicotine (figure 2-1).6 For example, enhanced release of dopamine, norepinephrine, and seroto- FIGURE 2-1  Source: Adapted from Pomerleau, O.F., and C. S. Pomerleau. "Neuro-regulators and the Reinforcement of Smoking: Towards a Biobehavioral Explanation." Neuroscience Behavioral Review 8 (1984): 503-513.

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Page 35 nin may be associated with pleasure as well as appetite suppression, the latter of which may contribute to lower body weight. Release of acetylcholine may be associated with improved performance on behavioral tasks and improvement of memory. Release of beta-endorphin may be associated with reduction of anxiety and tension. Tolerance and Withdrawal With prolonged or repetitive exposure to nicotine, the brain cells adapt in such a way as to compensate for the actions of nicotine, that is, to return brain functioning to normal. This process is called neuroadaptation. Neuroadaptation is associated with an increasing number of nicotinic receptors in the brain. Neuroadaptation results in the development of tolerance, that is, a given level of nicotine comes to have less of an effect on the body, and higher levels of nicotine are needed to produce the effects that lower doses formerly produced. Substantial tolerance develops to the behavioral arousal and cardiovascular effects of nicotine when a person smokes multiple cigarettes or uses multiple doses of smokeless tobacco, even within the course of a single day. Regular tobacco users regain sensitivity to the effects of nicotine, at least in part, after overnight abstinence from tobacco. When the brain has adapted so as to function normally in the presence of nicotine, it also becomes dependent on the presence of nicotine for normal functioning. When nicotine is not available (such as when a smoker stops smoking), the brain function becomes disturbed, resulting in a number of withdrawal symptoms, as mentioned above. Absorption of Nicotine from Tobacco Nicotine from tobacco smoke is rapidly absorbed into the systemic circulation after inhalation, then is quickly carried to various body organs including the brain. Nicotine levels in the blood rise quickly after smoking, with arterial blood levels exceeding venous levels in the first few minutes (figure 2-2). Because nicotine is a weak base and is ionized at acid pH, there is little absorption of nicotine through the membranes of the mouth from the acidic smoke of blond (light-colored) tobacco. However, the smoke of pipes, cigars, and dark tobacco is more alkaline, so nicotine is absorbed through the mouth from these products. When oral snuff or chewing tobacco is used, nicotine is also absorbed through the mouth. Nicotine from oral snuff or chewing tobacco is absorbed more slowly than from cigarette smoke; peak plasma concentrations of nicotine in venous blood are similar.

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Page 36 FIGURE 2-2  *Average values for 10 subjects. Shaded bars show the period of tobacco (or nicotine) use. Vertical bars indicate ranges. Source: Adapted from Benowitz, Neal L., H. Porchet, L. Sheiner, and P. Jacob III. "Nicotine Absorption and Cardiovascular Effects with Smokeless Tobacco Use: Comparison to Cigarettes and Nicotine Gum." Clinical Pharmacology and Therapeutics (1988): 23-28. Distribution and Elimination of Nicotine from the Body A cigarette delivers nicotine to the brain within 10 to 19 seconds from the start of a puff. The rapid passage of nicotine from the lungs to the arterial circulation to the brain provides for rapid behavioral reinforcement for smoking and for the possibility for the smoker to control levels of nicotine in the brain and to modulate pharmacologic effects. Nicotine is also distributed extensively to other body tissues. Slow release from tissues explains in part the elimination half-life of 2 to 3 hours. Nicotine is eliminated primarily by liver metabolism. The rate of metabolism is quite variable from person to person, so the same level of nicotine intake

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Page 37 may be associated with different concentrations of nicotine in the blood of different people. The main metabolite of nicotine, cotinine, has a long half-life (on average 17 hours) and has been widely used by researchers as a biochemical marker of nicotine exposure. Intake and Accumulation of Nicotine During Cigarette Smoking On the average, smoking a cigarette results in the absorption into the blood stream of about I mg of nicotine, but the range is from 0.5 to 3.0 mg. The elimination half-life of nicotine is 2 to 3 hours. This means that the level of nicotine in the blood decreases by one-half every 2 or 3 hours. It also means that after a single use of tobacco nicotine remains in the body for 8 to 12 hours. With repeated smoking, nicotine levels accumulate over 6 to 8 hours, plateauing through the remainder of the day, then gradually falling overnight. Thus, regular cigarette smoking results in continued exposure of the brain and body to nicotine. Addiction and the Light or Occasional Smoker Among adults the light or occasional smoker, that is, one who regularly smokes 5 or fewer cigarettes per day or who does not smoke every day, is in general less addicted than are daily smokers of more than 5 cigarettes per day.7 Smoking appears to be reinforced for light smokers by the direct pharmacologic effects of nicotine, as described above, as well as by behavioral aspects of tobacco use, as described below. The use of tobacco in response to withdrawal symptoms is less of a factor in such tobacco users. Among adults, light or occasional smokers are relatively uncommon (less than 10% of adult smokers);8 they have higher success in smoking cessation than do heavier smokers, although not all light smokers are able to quit. In contrast, many more children than adults are light or occasional smokers; however, light smoking by children is often not a stable pattern but, rather, represents a stage in escalation to becoming daily smokers. Nicotine Compensation The "Low-Yield" Cigarette Some tobacco advertisements indicate that particular brands of cigarettes deliver less nicotine and tar than their competitors' brands, implying a health benefit to low-yield cigarettes. Some people switch to low-yield cigarettes in an attempt to reduce the health consequences of smoking, but that is an unlikely result. A daily smoker tends to regulate his or her nicotine intake to a specific level in order to achieve desired effects and to minimize withdrawal symptoms.

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Page 38 This nicotine regulation influences how smokers smoke cigarettes with various nicotine yields and how they respond to cutting down on the number of cigarettes they smoke per day. When smoking lower-yield cigarettes, smokers puff more frequently or more intensely than when smoking higher-yield cigarettes, presumably to obtain their usual specific level of nicotine from each cigarette. In switching from high-yield to low-yield cigarettes, smokers consume more nicotine from the low-yield cigarette than predicted by smoking machine tests. Conversely, smokers consume less nicotine than predicted from high-yield cigarettes. The intake of nicotine, with blood cotinine or nicotine concentrations used as markers of nicotine intake, has been studied in large groups of people smoking their chosen brands of cigarettes.9 In such studies, nicotine intake correlates only weakly with the advertised yield. The slope of the regression line between advertised nicotine yields and blood nicotine or cotinine levels is shallow, suggesting only small differences of intake from cigarettes of widely different nicotine yields. Because of this compensatory smoking, having smokers switch to low-yield cigarettes reduces the risk of smoking to a much lesser degree, if at all, than suggested by the decreases in yield. Smoking Fewer Cigarettes The regulation of nicotine intake by daily smokers is also apparent when the number of cigarettes available to a smoker is restricted. In one study of heavy smokers, when the number of cigarettes was reduced from unlimited (average 37 per day) to 5 cigarettes per day, the average intake of nicotine per cigarette tripled.10 As a result, reducing the number of cigarettes to 15 per day had very little effect, and reducing to 5 cigarettes per day reduced the daily exposure to tobacco toxins only by 50%. This observation explains why many smokers who are instructed to quit report cutting down to about 10 cigarettes per day, but cannot reduce their consumption to fewer than 10. At 10 cigarettes per day smokers still can absorb adequate nicotine to maintain nicotine addiction. Behavioral Aspects of Addiction The behavior of smoking is maintained both by the direct pharmacologic effects of nicotine (including relief of withdrawal) and by learned responses. Anticipatory responses develop as a consequence of repetitive use of tobacco during which various kinds of gratifications from smoking occur in the presence of specific cues from the environment. For example, when a smoker encounters stressors or situational reminders of smoking, these stimuli revivify the pleasurable or other reinforcing aspects of smoking, which then generate the urge to smoke. Such recurrent anticipatory responses may persist 6 months or longer after physical dependence has been overcome, accounting for the relapses that

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Page 39 occur beyond the first week or two after cessation of tobacco use. Such anticipatory responses probably also develop to some degree in occasional smokers. There are various conceptualizations of the nature of the anticipatory response system. One is the conditioning model, in which learned associations between the effects of cigarette smoking and specific cues in the environment motivate smoking. Another model is self-regulation, in which high-risk situations activate cognitive processes in a form of pleasurable expectations and a reduced sense of personal control, which then increases the likelihood of smoking.11 Examples of common anticipatory reactions include smoking after a meal, with a cup of coffee or an alcoholic beverage, during a break from work, while talking on the phone, or while with friends who smoke. Of note, aspects of the drug-taking behavior itself often become pleasurable in addition to the pleasure afforded by the pharmacologic effects of nicotine. For example, manipulation of smoking materials or the taste, smell, or feel of tobacco smoke in the throat can become associated with the reinforcing effects of smoking and can become pleasurable in themselves. When a smoker becomes abstinent, he or she must learn not only to forego the pharmacologic pleasures afforded by the drug, but also the pleasure of engaging in those aspects of drug-taking behavior that have become pleasurable through anticipatory mechanisms. Behavioral factors other than anticipatory mechanisms may also influence personal susceptibility to drug addiction. For example, some smokers, particularly Caucasian women, smoke as a means of maintaining lower body weight.12 Certain characteristics of individuals appear to promote initiation of smoking and the development of nicotine addiction, as reviewed in more detail in a later section. Addiction to Smokeless Tobacco ''Smokeless tobacco" (SLT) refers to oral and nasal snuff and chewing tobacco. Smokeless tobacco, commonly used by youths, particularly in rural areas, may be highly addicting.13 Considerable nicotine is absorbed from smokeless tobacco. A classification scheme for levels of SLT use or addiction is problematic. The nicotine content of smokeless products is not known to the public and the nicotine content of the tobacco provides only a rough estimate of actual nicotine intake. Recent laboratory analysis of popular brands of moist snuff revealed large differences in nicotine content, from 5.7 to 30.7 mg/g.14 Two studies found evidence for higher addiction levels and greater oral pathology among Copenhagen® users.15 The systemic dose of nicotine derived from smokeless tobacco can be estimated by measuring blood nicotine levels after SLT use. The systemic dose of nicotine from snuff is 3.6 mg, and for chewing tobacco it is 4.5 mg; an average dose from smoking a cigarette is I mg.16 No standard self-report measures exist for smokeless tobacco consumption, such as those for smoking. One way to estimate addiction level is to use the number of

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Page 58 Hispanics.59 The reasons for ethnic differences in tobacco use among youths are unclear. Use of Smokeless Tobacco by Children and Youths Initiation of smokeless tobacco use begins in the preteen and early teen years. In 1991 smokeless tobacco was used by about 11% of high school seniors (table 2-11). The prevalence of smokeless tobacco use varies considerably in different regions of the country, with lowest rates generally in the Northeast, and lower rates in cities than in rural areas. Of note, the prevalence of smokeless tobacco use is greater than that of cigarette smoking by youths in several states, including Alabama, Idaho, South Dakota, Colorado, Wyoming, and Montana. The prevalence of moist snuff tobacco use by youths has risen dramatically, with a 10-fold increase for 16- to 19-year-olds between 1970 and 1985.60 There was a brief reduction in 1986-87, but sales of smokeless tobacco products are now increasing, with a 70% overall increase in moist snuff sales from 1982 to 1992.61 Smokeless tobacco is used primarily by males in all ethnic groups except American Indians and Alaskan natives, where the prevalence of use is similar for males and females. As discussed earlier, nicotine and cotinine concentrations in the blood of adults who use smokeless tobacco are comparable to those measured in smokers. No such data are available for children. Addiction of youths to smokeless tobacco is documented by reports that many users of smokeless tobacco have tried to quit but have been unsuccessful. According to the 1986-1989 Teenage Attitudes and Practices Survey, 21% of current smokeless tobacco users (12- to 18-year-olds) had tried to quit four or more times unsuccessfully, which is consistent with a high level of addiction.62 Factors influencing the initiation of smokeless tobacco are in general similar to those that are associated with initiation of cigarette smoking.63 One difference of note, however, is that smokeless tobacco use has been associated with participation on sponsored athletic teams (for example, baseball, wrestling, football, rodeo), whereas smokers are less likely to participate in such teams. As noted earlier, smokeless tobacco use is a risk factor for cigarette smoking, and vice versa. The exchangeability of tobacco use supports the idea that nicotine addiction can be maintained by tobacco from any source. NATURE OF TOBACCO PRODUCTS Nicotine addiction is maintained by use of tobacco, the only significant source of nicotine. Certain teas and vegetables contain low levels of nicotine, but the amounts available are so low that it is impossible to consume pharmacologically active doses of nicotine from sources other than tobacco. Tobacco is smoked as cigarettes, cigars, and in pipes, but can also be used

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Page 59 TABLE 2-11  Percentage of youths who currently (within the past 30 days) use smokeless tobacco Characteristic Monitoring the Future Project 1992a Youth Risk Behavior Survey 1991b Overall 11.4 10.5 Gender         Boys 20.8 19.2     Girls 2.0 1.3 Race/Hispanic origin         White, non-Hispanic 13.5 13.0         Boys 23.9 23.6         Girls 2.5 1.4     African American, non-Hispanic 2.5 2.1         Boys 5.2 3.6         Girls 0.2 0.7     Hispanic NA 5.5         Boys NA 10.7         Girls NA 0.6 Age         12-14         15-16         17-18     Grade          8th 7.0        9th   9.0     10th 9.6 10.1     11th   12.1     12th 11.4 10.7 Region         Northeast 8.2 8.8     North Central 12.3 13.3     South 12.5 8.6     West 11.1 10.5 a1992 MTFP survey of high school seniors. Based on responses to the question, "How frequently have you taken smokeless tobacco during the past 30 days?" With the exception of data for eighth and tenth grade students, all other data points for the Monitoring the Future Project survey reflect estimates for high school seniors. b Grades 9-12. Based on responses to the question, "During the past 30 days, did you you use chewing tobacco, such as Redman, Levi Garett, or Beechnut, or snuff, such as Skoal. Skoal Bandits. or Copenhagen?" Source: Centers for Disease Control and Prevention. Preventing Tobacco Use Among YoungPeople. A Report of the Surgeon General. Washington, DC: U.S. Department of Health and Human Services, 1994. 98.

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Page 60 without smoking by applying smokeless tobacco directly to mucous membranes. Several types of smokeless tobacco are available—oral snuff, nasal snuff, and chewing tobacco. Production of Tobacco Products Tobacco products in the United States are made by blending different types of tobacco leaf, to which sugar and other flavorings are added. Lighter tobaccos, which are found in most American cigarettes, produce acidic smoke when burned. Darker tobaccos, such as are used in cigar and pipe tobacco, produce alkaline smoke. As discussed elsewhere, the pH of the smoke determines the extent to which nicotine will be absorbed through the mouth. In addition to different types of shredded tobacco leaf, tobacco sheet or reconstituted tobacco is also blended into many cigarettes. Tobacco sheet uses scraps and stems of tobacco as well as various additives, which are combined into a homogeneous mixture that can then be incorporated into tobacco. The manufacturing of tobacco sheet allows for production of a relatively uniform composition of tobacco, since additives can be used to achieve the end product.64 Reports have been made of evidence that tobacco manufacturers manipulate the nicotine content of cigarettes.65 One way in which manufacturers control the nicotine content of tobacco is by extracting the nicotine from the tobacco, then adding it back in controlled amounts as tobacco extract. Tobacco companies also hold patents for spraying nicotine solutions onto cigarette tobacco, although it is unclear if this practice is actually used in the manufacturing of cigarettes. Tobacco manufacturers state that the reason nicotine is extracted and then reapplied to tobacco is that nicotine in the natural tobacco leaf exists in very uneven concentrations. By extracting and re-adding nicotine, it is possible to provide a more consistent tobacco product, which delivers a consistent amount of nicotine. It has also been suggested that the amount of nicotine in tobacco is controlled so as to ensure a level adequate to maintain nicotine addiction. In support of this idea was an internal memorandum, discovered in recent ligitation, from a Phillip Morris Tobacco Company scientist: "The cigarette should be conceived not as a product but as a package. The product is nicotine . . . smoke is beyond question the most optimized vehicle of nicotine and the cigarette is the most optimized dispenser of smoke."66 That the pharmacologic actions of nicotine are important determinants of why people smoke is supported by research both by the tobacco industry and by non-industry researchers.67 In the United States, four primary types of smokeless tobacco are manufactured: loose leaf, plug, twist or roll, and oral snuff.68 Loose leaf chewing tobacco consists of tobacco leaf that has been heavily treated with licorice and sugars. Plug tobacco is produced from leaves that are immersed in a mixture of licorice and sugar and then pressed into a plug. Twist tobacco is made from leaves that are flavored and twisted to resemble a rope. Oral snuff is available in

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Page 61 dry and moist preparations. Dry snuff is powdered tobacco that contains flavor and aroma additives. Moist snuff consists of fine particles of tobacco that contain considerable moisture; many varieties are prepared with flavorings such as wintergreen or mint. The oral use of snuff, called "snuff dipping," involves placing a pinch of the tobacco between the cheek or lips and the gum, or beneath the tongue. Starter products and distribution of free samples might introduce users to a graduation process of moving from low-nicotine to higher-nicotine snuff products. For example, products low in nicotine and low in pH (which reduces buccal absorption) and products sold in a teabag-like unit dose, would make it easier for first-time users to adapt to snuff products. The use of such low-nicotine-delivery products could be the beginning of a graduated process toward nicotine addiction. Modifying Cigarette Yields Tobacco smoke contains more than 4,000 chemicals, many of which are known toxins. Some of the better-known toxins include carbon monoxide, hydrogen cyanide, nitrogen oxides, ammonia, benzene, formaldehyde, nitrosoamines, vinyl chloride, polycyclic hydrocarbons, polonium-210, arsenic, and lead. Tobacco smoke is an aerosol of droplets containing water, nicotine, and other alkaloids, and tar. Tar is what is left in the particulates after water and alkaloids are removed. Particulates are suspended in a gaseous mixture, which contains carbon monoxide, nitrogen oxides, and other gases. To estimate the amount of various constituents that smokers are exposed to, cigarettes are routinely tested with a standardized smoking machine test. This test has been referred to as the Federal Trade Commission (FTC) method. The FTC performed and published test results in commercial cigarettes from 1967 until 1985; since that time the tobacco industry has conducted these tests. The FTC test procedure consists of placing a cigarette into a holder and igniting it; then 35-ml puffs are taken via a syringe over 2 seconds, once every minute until the cigarette is burned to a specific butt length. The smoke that is collected is passed through a filter to collect the particulate material (tar and nicotine). The gases that pass through the filter are collected for determination of carbon monoxide and other constituents. Thus, values for yields of tar, nicotine, and carbon monoxide for each cigarette are reported from this type of testing procedure. Lowering the yields of tar and other toxic constituents of cigarettes smoke makes intuitive sense as a way to reduce the health risks of cigarette smoking. Tobacco companies widely promote cigarettes that are lower in yield, implying a health benefit compared to smoking higher-yield cigarettes. However, the low-yield cigarette concept is in many ways deceptive. To understand why this is so, it is useful to examine how low-yield cigarettes are engineered.

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Page 62 There are several ways in which cigarettes can be engineered to be low-yield by smoking machine tests. The most obvious way is filtration, in which case a filter is placed at the end of the cigarette. This filter can remove a significant amount of tar. In the United States, 95% of cigarettes are filtered. Another way to reduce yields is to reduce the content of nicotine or other toxic substances in tobacco per se. This appears not to be the case with commercial cigarettes. When the nicotine concentration of tobacco in cigarettes of differing yields was measured, it was found that, on average, cigarette tobacco had a nicotine concentration of about 1.6%.69 There was a significant inverse correlation between concentration of nicotine in tobacco and yield, suggesting that low-yield cigarettes are made with tobacco that contains more, rather than less, nicotine than higher-yield cigarettes. In any case, it is clear that low-yield cigarettes are not low-yield because the contents of nicotine or tar are lower in the tobacco per se. Low-yield cigarettes are engineered to be low-yield based on the standardized smoking machine protocol. This can be done by shortening the cigarette length, increasing the burn rate of the paper, or increasing the length of the filter overwrap so that the machine is able to take fewer puffs before the cigarette is burned to its specified length. Placing less tobacco in each cigarette by using expanded tobacco and/or smaller diameters of cigarettes can also reduce yield. Diluting the mainstream smoke through the use of porous paper or ventilation holes in the filter tipping paper can substantially reduce yields. In the latter case, when the cigarette is inhaled from the tip, considerable room air is drawn in to dilute the tobacco smoke. Unfortunately, the addicted smoker does not smoke like an FTC smoking machine. Smokers take deeper and more frequent puffs than the machine on average, and can easily alter their smoking behavior as desired. Smokers learn, without realizing what they are doing, that placing their lips or fingers over the cigarette tip improves the draw characteristics of the cigarette. They are actually blocking the ventilation holes so that they are inhaling more tobacco smoke and less room air. Many studies in which the actual intake of nicotine, carbon monoxide, or other constituents of tobacco smoke have been measured in smokers, have shown a very weak relationship, if any, to nominal nicotine yield. Thus, once a smoker becomes addicted to nicotine, he or she can easily adapt smoking behavior to obtain the desired dose of nicotine from any cigarette. Of note, the ultra-low-yield cigarettes (that is, tar less than 1 mg, nicotine less than 0.1 mg) do seem to make it more difficult for smokers to obtain levels of nicotine that they can from high-yield cigarettes.70 The observation that sales of these ultra-low-yield cigarettes are relatively low suggests that there may be a threshold for nicotine delivery, below which nicotine addiction is not easily maintained. As typically smoked, low-yield cigarettes are not less harmful than higher-yield cigarettes. Because smokers take in much more tar and other toxins than estimated by machine yields, the risk of smoking-caused disease is not significantly reduced by using low-yield cigarettes.

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Page 63 In summary, people smoke cigarettes largely to obtain the nicotine they desire. They do not smoke in a standardized way as do smoking machines, and therefore machines are poor predictors of actual human exposure. Human exposures can be estimated by direct measures of levels of tobacco smoke constituents in biological fluids of smokers. Such markers include nicotine, its metabolite, cotinine, carbon monoxide, adducts of various reactive chemicals to hemoglobin or DNA, and mutagenic activity of the urine. CONCLUSIONS AND RESEARCH RECOMMENDATIONS Having reviewed the research literature on nicotine addiction and tobacco use, the committee finds the following conclusions to be warranted: 1. Long-term tobacco use is maintained by addiction to nicotine. 2. Use of any form of tobacco can result in addiction, and smokeless tobacco is becoming an increasingly prevalent behavior among youths. Smokeless tobacco is not a healthful alternative to cigarettes. 3. Once addicted, a person finds it difficult to quit using tobacco. 4. Children and youths begin tobacco use. Youths rapidly become addicted to nicotine; the addiction maintains their tobacco use in adulthood. 5. When youths begin using tobacco, they overestimate the proportion of tobacco use in society, underestimate the addictive nature of tobacco and the risk that they will become addicted over a long term, and underestimate the danger that they will incur tobacco-related disease. Thus, children and youths become addicted to nicotine before they are able to appreciate fully the consequences of their behavior. 6. There is considerable individual variation in susceptibility to nicotine addiction. Environmental, behavioral, personal, socioeconomic, and ethnic factors influence susceptibility to initiation and addiction. 7. The recognition that youths become addicted to nicotine should be incorporated into the design, evaluation, and dissemination of treatment programs for youths to stop tobacco use; as proven strategies emerge, they should be made easily accessible to youths. 8. Among adults the prevalence of cigarette smoking has declined from 1966 to the present. The prevalence of smoking by youths declined through 1980, but subsequently has been stable, except for African-American youths, for whom there has been a sharp decline. The prevalence of smokeless tobacco use by boys has increased steadily for the past 15 years and represents a significant growing addiction to tobacco. 9. Available evidence indicates that cigarette manufacturers control the level of nicotine in cigarettes and the nicotine delivery of their products in deliberate ways. However, "low-yield" cigarettes are not low in nicotine content and do

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Page 64 not in general deliver less nicotine or tar to smokers than do higher-yield cigarettes. 10. Prevention of nicotine addiction among youths is an essential part of any policy for reducing tobacco use in society as a whole. Approaches to prevention can be targeted toward the various factors that initiate and maintain tobacco addiction, as will be discussed in subsequent chapters. The Committee makes the following recommendations for research on nicotine addiction: 1. Research should be conducted to determine individual susceptibility to nicotine addiction. Particular areas that need research are genetic factors, affective states, and ethnic influences. Such information could facilitate the identification of high-risk children and could lead to more effective prevention strategies. 2. For all forms of tobacco products, research should be conducted on the characteristics of nicotine addiction in the early stages, that is, in the first few years during which the transition between experimental and addictive nicotine use occurs. Such information could contribute to more effective intervention before youth become highly addicted adult tobacco users. 3. Research should be conducted on the relationship between the characteristics of tobacco products and addiction. For example, as a basis in developing regulatory guidelines, it would be useful to know the minimal level of nicotine delivery from a tobacco product at which addiction will develop and/ or be sustained. REFERENCES 1. Chassin, L., C. C. Presson, S. J. Sherman, and D. A. Edwards. "The Natural History of Cigarette Smoking: Predicting Young-Adult Smoking Outcomes from Adolescent Smoking Patterns." Health Psychology 9:6 (1990): 701-716. 2. Tailoi, E., and E. L. Wynder. "Effect of the Age at Which Smoking Begins on Frequency of Smoking in Adulthood." New England Journal of Medicine 325:13 (1991): 968-969. 3. Edwards, G., A. Arif, and R. Hadgson. "Nomenclature and Classification of Drug- and Alcohol-Related Problems: A Shortened Version of a WHO Memorandum." British Journal of Addiction 77:1 (1982): 3-20. 4. Centers for Disease Control. The Health Consequences of Smoking: Nicotine Addiction. A Report of the Surgeon General. USDHHS (CDC) Pub. No. 88-8406. Washington, DC: U.S. Government Printing Office, 1988. 6-17; and Benowitz, Neal L. "Pharmacology of Smokeless Tobacco Use: Nicotine Addiction and Nicotine-Related Health Consequences." In Smokeless Tobacco or Health. An International Perspective. Smoking and Tobacco Control Monograph 2. NIH Pub. No. 92-3461. Washington, DC: National Cancer Institute, 1992. 219-228. 5. Gritz, Ellen H., C. R. Carr, and A. C. Marcus. "The Tobacco Withdrawal Syndrome in Unaided Quitters." British Journal of Addiction 86:1 (1991): 57-69. 6. Pomerleau, O.F., and C. S. Pomerleau. "Neuroregulators and the Reinforcement of Smoking: Towards a Biobehavioral Explanation." Neuroscience Biobehavioral Reviews 8:4 (1984): 503-513.

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Page 67 in Sixth Through Twelfth Grades." Addictive Behaviors 14:4 (1989): 365-378; and Ary. Dennis V., and A. Biglan. "Longitudinal Changes in Adolescent Cigarette Smoking Behavior: Onset and Cessation." Journal of Behavioral Medicine 11:4 (1988): 361-382. 47. Centers for Disease Control and Prevention. Preventing Tobacco Use, 123. 48. Perry, Cheryl L., and G. L. Silvis. "Smoking Prevention: Behavioral Prescriptions for the Pediatrician." Pediatrics 79:5 (1987): 790-799; van Teijlingen, Edwin, and J. A. Friend. "Children and Smoking: The Problem and the Way Forward." Thorax 47:7 (1992): 485-488: and Centers for Disease Control and Prevention, Preventing Tobacco Use, 123-146. 49. Glassman, A. H., J. E. Helzer, L. S. Covey, L. B. Cottler, F. Stetner, J. E. Tipp, and J. Johnson. "Smoking, Smoking Cessation, and Major Depression." Journal of the American Medical Association 254:12 (1990): 1546-1549; Anda, R. F., D. F. Williamson, L. G. Escobedo, E. E. Mast, G. A. Giovino, and P. L. Remington. "Depresssion and the Dynamics of Smoking: A National Perspective." Journal of the American Medical Association 264:12 (1990): 1541 - 1545: and Breslau, Naomi, Marlyne Kilbey, and Patricia Andreski. ''Nicotine Dependence, Major Depression, and Anxiety in Young Adults." Archives of General Psychiatry 48 (1991): 1069-1074. 50. Hirschman, Robert S., H. Leventhal, and K. Glynn. "The Development of Smoking Behavior: Conceptualization and Supportive Cross-Sectional Survey Data." Journal of Applied Social Psychology 14:3 (1984): 184-206. 51. Carmelli, D., G. E. Swann, D. Robinette, and R. Fabsitz. "Genetic Influence on Smoking—A Study of Male Twins." New England Journal of Medicine 327:12 (1992): 829-833. 52. Swan, G. E., D. Carmelli, R. H. Rosenman, R. R. Fabsitz, and J. C. Christian. "Smoking and Alcohol Consumption in Adult Male Twins: Genetic Heritability and Shared Environmental Influences." Journal of Substance Abuse 2:1 (1990): 39-50. 53. Hirschman et al. 54. Johnston, Lloyd D., P. M. O'Malley, and Jerald G. Bachman. Smoking. Drinking, and Illicit Drug Use Among American Secondary School Students, College Students, and Young Adults. 19751991. Volume I, Secondary School Students. NIH Pub. No. 93-3480 Washington, DC: National Institute on Drug Abuse, 1992. 64. 55. Johnston, Lloyd D., P. M. O'Malley, and Jerald G. Bachman. Monitoring the Future Project. Institute for Social Research. University of Michigan, 1994. Unpublished data. 56. Robinson, Robert G., Michael Pertschuk, and Charyn Sutton. "Smoking and African Americans." In Samuels, Robert G., Michael Pertschuk, and Charyn Sutton. eds. Improving the Health of the Poor: Strategies for Prevention. Menlo Park, CA: Henry J. Kaiser Family Foundation, May 1992. 131. 57. Wagenknecht, L. E., G. R. Cutter, N. J. Haley, S. Sidney, T. A. Manolio, G. H. Hughes, and D. R. Jacobs. "Racial Differences in Serum Cotinine Levels among Smokers in the Coronary Artery Risk Development in (Young) Adults Study." American Journal of Public Health 80:9 (1990): 1053-1056. 58. Centers for Disease Control. "Smoking Cessation During Previous Year Among Adults—United States, 1990 and 1991." Morbidity and Mortality Weekly Report 42:26 (1993): 504-507. 59. Schinke, S. P., R. F. Schilling, II, L. D. Gilchrist, M. R. Ashby, and E. Kitajima. "Native Youth and Smokeless Tobacco: Prevalence Rates, Gender Differences, and Descriptive Characteristics." NCI Monographs 8 (1989): 39-42; and Centers for Disease Control and Prevention, Preventing Tobacco Use, 97. 60. Marcus, Alfred C., L. A. Crane, D. R. Shopland, and W. R. Lynn. "Use of Smokeless Tobacco in the United States: Recent Estimates from the Current Population Survey." Smokeless Tobacco Use in the United States. NCI Monographs 8 (1989): 17-23. 61. Sullivan, Louis W. "Keynote Address." In Smokeless Tobacco or Health: An International Perspective. Smoking and Tobacco Control Monograph 2. NIH Pub. No. 92-3461. National Cancer Institute, 1992. iv. 62. Centers for Disease Control and Prevention. Preventing Tobacco Use. 101.

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