Smokeless tobacco: epidemiology, health effects and cessation strategies - includes patient informat

Author: John G. Spangler, Paul Lee Salisbury, III
Date: Oct, 1995

Smokeless tobacco is a highly addictive substance containing several known carcinogens[1-3] Chewing tobacco (plug or loose leaf) and snuff (either dry or moist powder or powder in small sachets similar to tea bags) are the most common forms of smokeless tobacco (Figure 1).

While the prevalence of cigarette smoking is declining nationally,[4] the use of smokeless tobacco has almost tripled in the past 20 years.[5] Smokeless tobacco use has become especially common among adolescents, and some researchers are concerned that a future epidemic of oral cancers may occur in these individuals.[6] Smokeless tobacco use also remains high in certain demographic groups, such as Native Americans.

This article examines the epidemiology of smokeless tobacco use and its adverse health consequences. Prevention and cessation strategies that may be incorporated into family practice are also presented.


According to a 1991 survey,[7] smokeless tobacco is used by 2.9 percent of adult Americans (5.6 percent of all men and 0.6 percent of all women). Rates of use are highest in Native American adults (5.4 percent prevalence of use) and in adults residing in the South or in rural areas in various parts of the United States.

Smokeless tobacco is more frequently used by persons 18 to 24 years of age and, at the other end of the age spectrum, by those 75 years of age and older. Use is more prevalent among persons with less than 12 years of education and among those living below the poverty level.[7] The prevalence rates of smokeless tobacco use are also increased in areas with an economy based on tobacco production (e.g., rural North Carolina or Kentucky).[8,9]

The greatest increase in smokeless tobacco use in the past two decades has occurred among adolescents, with up to 24 percent of white male high school students identifying themselves as current users.[10] Risk factors for adolescent smokeless tobacco use include white[10] or Native American[11] race, male sex,[10] participation in organized baseball,[12] smokeless tobacco use by family members or peers, and use of other substances.[13]

The smokeless tobacco habits of Native Americans deserve special comment. Tobacco has been a part of Native American culture since before the arrival of Columbus.[14] Today, Native American young persons and adults have higher rates of smokeless tobacco use than their white, Hispanic or black counterparts. Prevalence rates range from 5 to 33 percent in various Native American populations.[7,11,15,16] Perhaps more worrisome than the high prevalence of use is the extremely young age at which many Native American children start using smokeless tobacco--in some cases before kindergarten.

Health Effects

The adverse health consequences of smokeless tobacco use can be broadly categorized into dental and oral soft tissue effects, including leukoplakia and oral cancer, and systemic effects mediated by nicotine.


The placement of smokeless tobacco adjacent to the teeth damages the gingiva and the periodontium[1,17] (rigure 2). Gingival recession usually involves one to four of the teeth that are immediately adjacent to the site at which the tobacco quid is habitually placed.[1] With habitual use, the gingival margin migrates from 1 to 8 mm down the root of the tooth, and inflammation may or may not be present.[17]

Surveys[18,19] involving hundreds of school-age smokeless tobacco users and baseball players have shown that gingival recession and loss of periodontal attachment are frequent sequelae of smokeless tobacco use. The risk of these oral problems is up to nine times higher in smokeless tobacco users than in nonusers.[18,19]

Gingival recession frequently occurs, even with adequate plaque removal, and the gingiva may not regenerate after cessation of smokeless tobacco use. Such permanent damage may require gingival grafting in some cases and may be completely irreparable in others.[1]

Most clinical evidence does not support a definite association between smokeless tobacco use and increased rates of dental caries.[17] However, chewing tobacco and snuff stain the teeth of 30 percent of users and abrade tooth structures in 15 percent of users.[19] Indeed, long-term intense use of grit-containing smokeless tobacco produces excessive wear of the tooth cusps and incisal edges (Figure 2)[17] Halitosis is also a problem with smokeless tobacco use.[1]


Oral leukoplakia is a "white plaque" that cannot be removed by scraping (Figure 3) and cannot be classified as any other disease, such as candidiasis.[18] The significance of leukoplakia is its frequent association with smokeless tobacco use and its 3 to 6 percent transformation rate to squamous cell carcinoma over time. For the latter reason, this lesion is termed "premalignant."[1,20] Carcinoma in situ and invasive carcinoma are not usually found in leukoplakias unless the lesion contains red-colored areas, referred to as erythroplakia or erythroplasia (Figure 4).

Under normal conditions, the oral mucosa is smooth and moist, with an almost transparent surface. However, smokeless tobacco use produces a white or yellowish-brown, wrinkled-appearing lesion in at least half of regular snuff users.[19,21] While cessation of use may lead to regression or complete resolution of leukoplakia, some lesions, especially the thicker ones, often remain.[17]

Leukoplakia induced by smokeless tobacco is almost always found where the mucosa of the cheek, alveolar ridge and gingiva have direct and prolonged exposure to the tobacco. In the United States, snuff users most often have lesions in the mandibular mucobuccal fold in the incisor and premolar regions, where the quid of tobacco is held. The lesions are usually solitary, approximate four or five teeth and have fairly diffuse borders with normal tissue.[18,19] Compared with snuff users, tobacco chewers have a much lower incidence of leukoplakia, and lesions in these patients are mostly seen in the buccal mucosa bilaterally.[17,19,22]

The management of leukoplakia begins with the removal of all oral irritants (e.g., dentures, smokeless tobacco use). After two weeks, the patient is reexamined to see if the condition has resolved. If leukoplakia persists, a biopsy should be performed.


Long periods of smokeless tobacco use can result in oropharyngeal cancer, as reported in a landmark case-control study[23] conducted in the early 1980s and in a recent survey of 128 patients with oral cancer.[21] In the latter study,[21] 93 percent of patients with oral cancer reported using snuff and 6 percent reported using chewing tobacco, with no other carcinogen exposure. Leukoplakia, erythroplakia or both were associated with 40 percent of tumors at presentation, and the diagnosis was squamous cell carcinoma in all but one patient. Almost all of the tumors were located in the buccal/labial vestibule, the site where the tobacco quid was held. In contrast, oral and pharyngeal cancers associated with exposure to other carcinogens, such as cigarettes or alcohol, occur on the tongue, the soft palate/tonsil or the floor of the mouth. Advanced oral cancers related to smokeless tobacco use are shown in Figures 5 and 6.

Like other oral cancers, the carcinomas induced by smokeless tobacco appear to have an aggressive course, with five-year survival rates of less than 50 percent.[21] Consequently, smokeless tobacco users with a history of oral cancer must have frequent and thorough examinations of the oral cavity for the rest of their lives, and especially during the first two years after treatment.[20,21]


Smokeless tobacco products generally contain a high concentration of nicotine, an extremely addictive substance. The typical single dose of nicotine in snuff is almost twice the dose in cigarettes, while the typical single dose of nicotine in chewing tobacco is over 15 times greater than the dose in cigarettes.[24] Regular users of smokeless tobacco often experience nicotine withdrawal symptoms on cessation.[25] Nicotine enhances the release of catecholamines, and it increases heart rate, contractility and blood pressure.[24] This substance adversely affects the lipid profile by raising the total cholesterol level and lowering the high-density lipoprotein cholesterol level through its effects on triglycerides.[26]

Nicotine also inhibits prostacyclin synthesis, which promotes platelet aggregation.[24] Taken together, these nicotinemediated effects can accelerate atherosclerosis of the coronary and peripheral vasculature and predispose smokeless tobacco users to thrombosis, myocardial infarction, hypertension and stroke.[24]

As a cholinergic agonist, nicotine exacerbates gastroesophageal reflux and peptic ulcer disease. It also delays wound healing. Use of this substance also contributes to perinatal morbidity, including low birth weight and prematurity.[24] Some athletes have cited enhancement of reaction time as a justification for smokeless tobacco use. However, this putative effect of nicotine has not been established experimentally.[1,27]

Smokeless Tobacco Cessation

Because heavy consumers of cigarettes and smokeless tobacco share nicotine dependence, strategies to help persons quit using smokeless tobacco have largely been adaptations of smoking cessation techniques.[28] An algorithm outlining one possible approach is presented in Figure 7.

In tobacco cessation counseling, the first step is to identify the tobacco use status of all patients and to record this information in the medical chart.[29] If the patient is a tobacco user, the form and the extent of use should preferably be noted in the patient's problem list. After determining the tobacco status, the physician must assess the patient's readiness to quit. The major theoretic models that can be used to make this determination is Prochaska and DiClemente's Stages of Change.[30] This model was developed with the realization that for cessation messages to be effective, they must be consistent with the patient's motivation to quit. Patients who have given no thought to quitting should be informed about the adverse health effects of smokeless tobacco use, with personalization of the message.

In a patient with leukoplakia, for example, the physician can emphasize this lesion's potential for malignant transformation, explaining its direct connection to smokeless tobacco use and the likelihood of its regression with tobacco cessation.

Patients who are unsure about their willingness to quit can be given so-called "intermediate" steps designed to focus their attention on their smokeless tobacco habit. Such steps might include keeping a tobacco diary in which they record the time of day and their feelings before each use, prohibiting themselves from using smokeless tobacco in specific places, such as their car, or simply cutting down on the amount of tobacco that they chew or dip each day. Patients already contemplating quitting or actively trying to quit need emotional support, and some may also require therapeutic support. At this point, the physician's task is to establish whether the patient is dependent on nicotine. This information can be used to determine whether the patient might benefit from nicotine replacement therapy and to provide anticipatory guidance regarding nicotine withdrawal symptoms.

We have developed a questionnaire to identify nicotine dependence in smokeless tobacco users (Figure 8). A total of l0 points are possible on the questionnaire, and a score of 6 or more indicates nicotine dependence. The questionnaire was derived from Fagerstrom's nicotine tolerance questionnaire,[31] a tool commonly used with smokers. A similar approach has also been reported by Eakin and co-workers.[32]

Long-term abstinence rates with nicotine replacement therapy have been disappointing.[1,28] Indeed, the vast majority of former smokers quit without nicotine therapy.[33] Furthermore, improper use of nicotine replacement products can cause adverse side effects that needlessly discourage the motivated active quitter.[28]

On the other hand, 2-mg nicotine polacrilex (Nicorette) or nicotine transdermal patches (Habitrol, Mcoderm, Prostep, etc.) may lessen nicotine withdrawal symptoms in selected nicotine-dependent patients, especially those who have experienced withdrawal symptoms in the past or whose previous attempts to cease tobacco use have been unsuccessful. Contraindications to the use of these products, as listed in package inserts, include pregnancy, angina, life-threatening arrhythmias and recent myocardial infarction. Patients must understand the importance of stopping tobacco use before starting nicotine replacement therapy. Potentially serious vasospastic events may occur with the concomitant use of tobacco and nicotine replacement products.

Regardless of the patient's willingness to quit or to use nicotine replacement products, follow-up is necessary in all smokeless tobacco users. Patients who are interested in smokeless tobacco cessation should be encouraged to set a quit date within one to two weeks of the current office visit and should have an appointment arranged near that quit date to reinforce compliance. The quit date should not be scheduled at a time of anticipated personal stress, such as a job promotion or school examinations.

Patients not currently interested in quitting should be told that tobacco cessation will be mentioned at future office visits. An office reminder system--even something as simple as flagging the chart-should be developed to ensure that the subject is discussed.[29] The family physician can offer patients other forms of support in their efforts to stop using smokeless tobacco. For example, since smokeless tobacco is an oral habit, certain patients may benefit from oral replacements (in addition to nicotine replacement therapy). Nicotine polacrilex has the advantage of being both an oral substitute and a therapeutic replacement of nicotine.[2,28] Some patients have found pumpkin or sunflower seeds, chewing gum or herbal "snuffs" to be helpful. Ground mint leaves have been a safe and appealing snuff substitute for some patients.[28,34] Anecdotal reports indicate that some patients have chewed caffeine free herbal tea bags during cessation attempts. Severson35 has developed a short, easily read self-help booklet that may be useful for persons who are motivated to quit smokeless tobacco use. The family physician can facilitate the support that the patient's family or friends give to the cessation effort. It is particularly effective for the patient to have a family member or friend quit chewing or dipping tobacco at the same time. The physician must remain alert to the possibility that a patient will switch from smokeless tobacco to another tobacco product, such as cigarettes. Unfortunately, substitution of one tobacco form for another form is common.[23] This potential problem should be mentioned when quitting is contemplated, and it should be addressed at follow-up visits with the active quitter. Side effects of tobacco cessation, such as irritability and nervousness, need to be anticipated, as should the possibility of relapse. Since smokeless tobacco users relapse as late as six months after their quit date,[1] follow-up should be continued for that time period or longer.

Finally, the family physician should provide smokeless tobacco counseling to adolescents in the same way that advice is given on cigarette smoking and alcohol use. The unambiguous message must be that there is no safe form of tobacco.[36] Pamphlets, posters, videos and office handouts to help the physician guide patients through the cessation process can be obtained from the National Cancer Institute, the American Cancer Society and other organizations (Table 1). In addition, a patient information handout on quitting smokeless tobacco use appears at the end of this article.


JOHN G. SPANGLER, M.D., M.P.H. is assistant professor in the Department of Family and Community Medicine at Bowman Gray School of Medicine of Wake Forest University in Winston-Salem, N.C. Dr. Spangler graduated from the University of North Carolina School of Medicine, Chapel Hill, completed a master's degree in public health and a preventive medicine residency at Johns Hopkins University, Baltimore, and served in a family medicine residency and a faculty development fellowship at the Bowman Gray School of Medicine.

PAUL LEE SALISBURY, III, D.D.S. is associate professor of dentistry at the Bowman Gray School of Medicine. Dr. Salisbury received his dental degree trom the University of North Carolina School of Dentistry, Chapel Hill, where he also completed a general practice residency and a fellowship in oral cancer. Address correspondence to John G. Spangler, M.D., M.P.H., Depaffment of Family and Community Medicine, Bowman Gray School of Medicine of Wake Forest University, Medical Center Boulevard, Winston-Salem, NC 27157-1084.

COPYRIGHT 1995 American Academy of Family PhysiciansCOPYRIGHT 2004 Gale Group

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