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Editors: Pamela Korsmeyer and Henry R. Kranzler
Date: 2009
Encyclopedia of Drugs, Alcohol & Addictive Behavior
Publisher: Macmillan Reference USA
Document Type: Topic overview; Brief article
Pages: 36
Content Level: (Level 5)
Lexile Measure: 1370L

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This entry includes the following essays:


The term tobacco generally refers to the leaves and other parts of certain South American plants that were domesticated and used by Native Americans for the alkaloid nicotine. Tobacco plants are a species of the genus Nicotiana, belonging to the So-lanaceae (nightshade) family, which also includes potatoes, tomatoes, eggplants, belladonna, and petunias. Including plants used for tobacco, there are 64 Nicotiana species. The two widely cultivated for use as tobacco are Nicotiana tabacum and Page 96  |  Top of ArticleNicotiana rustica, the latter of which contains the higher levels of nicotine.

Nicotiana tabacum is, however, the major source of commercial tobacco, although it has been hybridized with other Nicotiana species and its chemical composition altered in the process. Nicotiana tabacum is a broad-leaf plant that grows from three to ten feet (1–3m) tall and produces ten to twenty leaves radiating from a central stalk. Nicotiana rustica, also known as Indian tobacco, was first cultivated by Native Americans and was probably the tobacco offered to Columbus. The word tobacco came into English about 1565 from the Spanish word tabaco, which probably derives from the Taino word for the roll of leaves containing the N. rustica that the indigenous people of the Antilles smoked.


Tobacco was introduced to Europeans by Native Americans at the time Columbus explored the New World (1492–1506). The first written records of tobacco use date from this time, but there is archaeological evidence for tobacco's wide use in the Americas as early as 600 to 900 CE. Native Americans considered tobacco to be sacred, and the plant was used in social, fertility, and spiritual rituals. For example, tobacco was used for seasonal ceremonies, for sealing friendships, preparing for war, predicting good weather or good fishing, planting, courting, consulting spirits, and preparing magical cures. The desired effect of tobacco was a trance state, achieved by using the leaves in various ways, including smoking, chewing, snuffing, drinking (tobacco juice or tea), licking, and injecting in enemas.

Tobacco Use Spread from the Americas to Europe. Acute nicotine poisoning was a central aspect of the practice of shamanism in many parts of South America. South American shamans would smoke or ingest tobacco to the point of producing a nicotine-mediated trance or coma. The dose of nicotine could be titrated to produce a coma state resembling death, but from which the shaman would recover. Recovery from apparent death was believed to enhance the perception of the shaman's magical powers.

Tobacco use spread widely through all the Americas, and most tribes had ceremonial traditions related to tobacco. Although tobacco ceremonies were common among native tribes in the Americas from Canada to Argentina, the traditions and stories about the origin of tobacco vary greatly. In 1492 Columbus encountered natives in Hispaniola smoking tobacco in the form of large cigars. Enticed by the sacred and special regard in which they held tobacco, Columbus's crew experimented with tobacco smoking and soon became enthusiastic users. In the early 1500s tobacco cultivation began in Portugal. By the late 1500s, France had introduced tobacco cultivation to Holland and later to Italy. By 1570 tobacco had been introduced to Germany, Switzerland, Austria, and Hungary. In central Europe tobacco was primarily used for medicinal purposes. Tobacco was said to be useful in the prevention of plague and as a cure for headache, asthma, gout, ulcers, scabies, labor pains, and even cancer.

Objections by James I to Tobacco. In 1570 the tobacco plant was named Nicotiana after Jean Nicot, the French ambassador to Portugal who introduced tobacco to France. In the late 1500s, Sir Walter Raleigh popularized the smoking of tobacco for pleasure in the court of Queen Elizabeth I (reigned 1558–1603); from there it spread to other parts of England.

James I of England (reigned 1603–1625), who succeeded Elizabeth, was strongly opposed to tobacco use and in 1604 wrote the first major anti-tobacco treatise, A Counterblaste to Tobacco. King James described tobacco as “a custome loathsome to the eye, hateful to the nose, harmful to the brain, dangerous to the lungs, and in the black stinking fume thereof nearest resembling the horrible stygian smoke of the pit that is bottomless.” Despite James's opposition, however, tobacco use flourished. Eventually, even James lessened his opposition to tobacco because of the lucrative income from its taxation. Governments often became addicted to the tax revenues from tobacco much like people became addicted to the chemicals being taxed. These revenues were often used to fund wartime efforts and support the economy during desperate times (Courtwright, 2001, p. 156).

Throughout Europe pipe use became the popular method of consuming tobacco, and the first vending machine for pipe tobacco was introduced in England in 1610. During the Thirty Years War (1618–1648), which began as a struggle for Page 97  |  Top of Articlereligious supremacy that grew into a large-scale non-religious struggle for political dominance in Europe, tobacco use expanded primarily through the ranks of warring armies. With Germany being the primary battle area for the war, historians estimate that nine out of every ten peasant homes had a tobacco user (Corti, 1932, p. 108). Also during this time, medical practitioners began treating many common ailments with tobacco, leading to increased use of the pipe.

Tobacco as Big Business, and Its Critics. In the early 1600s, Spain, Portugal, and England increased their financial investment in tobacco through cultivation in their North American territories. In 1614, King Phillip III of Spain declared Seville the tobacco center of the world and had all Spanish crops in the Americas funneled through Seville. Simultaneously, the English expanded cultivation in their colony of Virginia. In 1619, the first slaves arrived in Virginia to cultivate English tobacco crops. Rapidly expanding tobacco production by the English was credited for the slave trade industry in the seventeenth and eighteenth centuries. Tobacco growers in the Americas realized that growing tobacco required large numbers of permanent laborers and found inexpensive labor from the Africans being shipped from West Africa. Although many were originally brought to the Americas as indentured servants, the practice transformed into slavery as profit-minded plantation owners institutionalized the practice of owning permanent laborers and providing only for their basic needs plantation owners.

Throughout the 1600s increasing numbers of antismoking regulations spread throughout Europe and east to Russia. The Russian Czar Michael Feo-dorivich (1596–1645) declared tobacco use a deadly sin and established harsh punishments for offenders. Murad the Cruel of Turkey (1623–1640) ordered that tobacco users be beheaded, quartered, and/or hanged. As the anti-tobacco pressures increased in Europe and Russia, tobacco trade moved into Asia. By the mid-1600s, smoking was a pastime in China, Japan, Korea, and India. Shortly, antismoking pressures increased, leading Persia and India to enact death penalties for tobacco use. In 1620 Japan banned smoking for the first time. Nevertheless, smoking persisted. Government prohibitions became costly to national economies as the trade of tobacco moved to black markets. India's tobacco bans in the late 1800s alone created a significant negative impact on government revenue as tobacco revenue dropped from 14 percent in 1880 to 7 percent in 1905 (Courtwright, 2001, p. 183).

Due to the enormous profit in tobacco trade, smuggling and black markets for tobacco increased greatly during the 1700s. Ireland and Scotland became gateways for tobacco smuggling. Tobacco created an economic boom leading to population growth and prosperity in Glasgow. During the early 1700s, England's state of war with France and Spain contributed to Scotland and Ireland's prosperity in tobacco as their ports provided safer transport than England's.

Despite countervailing pressures, tobacco was also recognized as having medicinal properties. During an outbreak of the bubonic plague (Black Death) in England in the mid-1600s, tobacco was recognized as a preventive measure. Young men during this period were encouraged to smoke a daily pipe at Eton College and were routinely punished for not doing so.

Royal Support of Tobacco. During the 1700s, Europe saw a resurgence of tobacco use among European elites. Smoking had become primarily a pastime of the lower and middles classes following the Thirty Years War and the social elite turned to using tobacco in the form of snuff, a finely ground tobacco powder inhaled through the nose. Opposed to smoking, Louis XIV of France promulgated the use of snuff as a discreet habit that did not offend others with smoke. Snuff-taking throughout the 1700s increased dramatically. In contrast to most of Europe, Frederick I and Frederick William I of Prussia were avid pipe smokers who began the first tobacco club with the sole purpose of promoting smoking.


In France and England, snuff-taking continued to grow in popularity among the aristocracy. Even Napoleon I was rumored to consume up to seven pounds of snuff a month. Expensive to produce and package, snuff was used mostly by the upper classes. Snuff-taking was popular until the mid-1800s when smoking was reintroduced with the emergence of cigars from the Spanish colonies. Various ancestors Page 98  |  Top of Articleto the modern cigarette first appeared in the mid-seventeenth century. For example, the famed Casanova (1725–1798) in Italy helped popularize the hand-rolled cigarette. Not until 1843, however, did Manufacture Francaise des Tabacs produce the first commercial cigarette. Napoleon III (1808–1873) helped popularize the cigarette with his own 50-per-day habit. With the introduction of mass production of commercial cigarettes, large manufacturing plants began to appear in Europe and North America. In 1847 Phillip Morris opened his first production plant in England, producing hand-rolled Turkish cigarettes.

Tobacco production was a mainstay of American capitalism. In contrast to Europe, the U.S. public preferred chewing tobacco to smoking in the early 1800s. By 1860, the U.S. business census listed 348 tobacco factories producing chew tobacco in North Carolina and Virginia alone. However, cigar smoking also grew in popularity in the United States after soldiers in the Mexican War (1846–1848) returned with a desire for the darker, richer tobacco found in Latin cigars. Most tobacco was smoked as cigars or in pipes or used as snuff. Cigarettes were hand rolled. A skillful worker could roll four cigarettes per minute. Cigarette smokers were primarily boys or women, and smoking was a behavior confined to the lower socioeconomic class.

The gold rush of 1849 in California spurred an American interest in finer tobaccos and liquors. San Francisco became known as the capital for the best bad things in the United States. The Civil War contributed to the U.S. growth in tobacco consumption in two ways. First, the ration packs for soldiers in both the Confederate and Union armies contained tobacco products. Second, the U.S. government imposed the first excise tax on tobacco to help fund the Civil War for the Unionists.

Introduction of the match in 1852 and mass production of commercial cigarettes caused cigarette consumption to rise in the latter half of the 1800s. Increased smoking led to resurgence in antismoking regulations. In 1868, the British Parliament banned smoking on all commercial trains. In 1871, the U.S. House of Representatives voted to ban smoking in its own chambers. The U.S. Senate was able to enact the ban in its chamber in 1914. Nonetheless, smoking prevailed.

Cigarette Rolling Machine. The invention of the cigarette rolling machine by James Bonsack in 1880 made tobacco use inexpensive and convenient. Bonsack went into business with W. B. Duke and Sons in Durham, North Carolina. Together they improved the machine; by April 30, 1884, the device could roll 120,000 cigarettes per day. Duke used his competitive edge in manufacturing with an exclusive agreement with Bonsack to drive the price down, making cigarettes more affordable for the general public. Duke's American Tobacco Company dominated tobacco through the late 1800s but eventually collapsed in an anti-trust action in 1911.

Popular Culture and the Cigarette. By the late 1800s, tobacco had entered the world of popular entertainment and had begun to appear in popular fiction. Mérimée's 1865 novel about a cigarette girl in Seville became the basis for the opera Carmen. In 1878, trading cards and coupons began to appear in packs of cigarettes. Sports figures became the first trading cards to link tobacco and celebrity. By the beginning of the 1900s cigarette consumption in the United States had increased more than fourfold. At the same time, chewing tobacco had reached its peak consumption.

Ironically, as pressures increased in the U.S. Congress to ban or control tobacco, the government listed tobacco in the U.S. Pharmacopoeia. This government endorsement of tobacco as a medicinal agent led to partnerships between the tobacco companies and the medical community. In 1899, the first Merck Manual, a widely used reference book for physicians, listed tobacco as a treatment for bronchial distress and asthma.

Mass media opened doors to tobacco never experienced before the first half of the twentieth century. The glamorization of cigarette smoking increased through the use of entertainment celebrities as spokespersons and the inclusion of smoking in the new motion picture industry. Both world wars provided a venue for increasing tobacco use by soldiers, who received cigarettes as rations. Tobacco advertising also included doctors among the role models depicted as smoking cigarettes. Despite the fact that tobacco had been removed from the U.S. Pharmacopeia by 1905, smoking was considered sophisticated, glamorous, individualistic, and even healthful. Across the world, the average person was spending 3 to 5 percent of his or Page 99  |  Top of Articleher total income on tobacco by 1951, according to John B. Hutson, president of Tobacco Associates in a paper published in that same year.


Strong opposition to tobacco consumption emerged by the turn of the twentieth century with 43 of the 45 states addressing tobacco as a menace. Business owners joined ranks in 1908 and began refusing employment for people who smoked. However, bans on sales of tobacco to minors were the only successful national regulation in the United States, Canada, and England. Despite antismoking regulations, tobacco consumption in the first half of the 1900s increased, peaking in 1955 in the United States with 50 percent of men smoking and in 1966 for women, with 32 percent of women smoking. By the 1960s nearly half of Americans were addicted to nicotine.

Health Hazards and Legal Action. While there had been occasional reports on the health hazards of cigarette smoking from the time of King James, the first large-scale studies documenting the link between cigarette smoking and cancer appeared in 1950 (Doll & Hill, 1950; Wynder & Graham, 1950). Subsequently, hundreds of studies have shown that cigarette smoking accounts for 30 percent of cancers—including some cancers of the lung, mouth, throat, esophagus, bladder, and kidney, as well as some leukemia; and that it is the cause of some heart and vascular disease, stroke, emphysema, chronic obstructive lung disease, and other health problems. The U.S. Office of the Surgeon General regularly publishes findings regarding the health consequences of tobacco use with the most comprehensive report released in 2004. The first comprehensive review of the scientific research regarding the health consequences for nonsmokers regularly exposed to smoke in their work, home, and social environments was published by the U.S. Office of the Surgeon General in 2006. This report has been paramount in supporting tobacco bans worldwide.

Unprecedented scientific and legal efforts to reduce the use of tobacco emerged in the second half of the twentieth century. With mounting support that tobacco causes different types of cancer, multiple lawsuits were filed in the 1950s in the United States against tobacco companies. The increase in scientific literature led to the 1962 report by the Royal College of Physicians in Britain and the 1964 Surgeon General's Report in the United States linking tobacco with lung cancer. The largest public health campaign related to any one issue began with these reports.

The 1960s in the United States started the era of comprehensive tobacco control. Regulations were passed that limited advertising by tobacco companies. Tobacco advertising on television was banned in the United Kingdom. Warning labels about the dangers of tobacco had to be placed on all tobacco products in the United States. The U.S. Surgeon General released three more reports on the dangers of smoking. By the 1970s legislation was introduced in the United States and the United Kingdom that banned smoking in public places, including airlines. Individual states within the United States began to draft legislation to control where people would be allowed to smoke.

During this same time, in stark contrast to many of the industrialized nations moving toward smoking bans, Japan stood out for its political support of smoking. Emperor Hirohito started a tradition of passing out cigarettes to all of his employees on his birthday. He also provided free cigarettes to the elderly on a holiday honoring them. Japan's consumption of tobacco peaked in 1966 with 84 percent of men smoking, according to the World Health Organization in 1998.

Federal Restrictions. In the 1990s the United States and other industrialized nations moved to reduce both the affordability and convenience of smoking. Federal and state governments began placing large taxes on tobacco products that significantly increased the cost of tobacco. With smoke-free laws being regulated, making smoking less convenient, more regular smokers quit. By the end of the 1990s, according to the Centers for Disease Control, smoking rates in the United States had dropped to about 25 percent in the adult population.

In 1997 the United States Attorney General's Office and the tobacco companies came to the largest agreement ever settled by the tobacco industry. The master settlement agreement severely restricted advertising, required bold warnings on tobacco, and limited damages against tobacco companies in lawsuits. The tobacco companies admitted they knew tobacco was addictive and company executives lied about the dangers of using tobacco.

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Tobacco control efforts had mixed impact in Asia. In 2000, Japan demonstrated the effect of pressures to control tobacco use as Emperor Akihito repealed the tradition of handing out cigarettes to staff on his birthday. Smoking rates dropped to 47.7 percent that year. With all the tobacco control efforts across the globe during this time, China National Tobacco Company accounted for 31 percent of the tobacco market, representing 385 million smokers in China in 2000, making it the dominant tobacco trader in the world.

In February 2005 the Framework Convention on Tobacco Control (FCTC) took effect in the 40 countries that ratified it. The convention sought to protect the world's citizens from the dangers of secondhand smoke. By 2008 over 65 countries had established smoke-free laws that limit or ban smoking in public places. In the United States, according to the 2007 Morbidity and Mortality Weekly Report, rates dropped from 25 percent in 1999 to 21 percent in 2004. In the United States smoking rates among teenagers dropped from 28 percent in 1991 to 23 percent in 2005. Although the overall smoking rate dropped through the early years of the twenty-first century, the U.S. Centers for Disease Control reported a disproportionate number of smokers among African Americans, Asian Americans, and the gay/lesbian populations.

While smoking rates continued to drop in industrial nations, WHO noted that smoking rates in developing countries were on the increase in the early years of the twenty-first century. With the increased restrictions for marketing in industrial nations, the largest tobacco companies looked elsewhere for profits, developing multinational offices to increase marketing efforts in developing markets.

See also Advertising and Tobacco Use; Nicotine; Nicotine Delivery Systems for Smoking Cessation.


Corti, C. (1932). A history of smoking. Translated by Paul England. New York: Harcourt, Brace and Company.

Courtwright, D. T. (2001). Forces of habit: Drugs and the making of the modern world. Cambridge, MA: Harvard University Press.

Doll, R., & Hill, A. B. (1950). Smoking and carcinoma of the lung: Preliminary report. British Medical Journal, 2, 739–748.

Gilman, S., & Zun, X. (2004). Smoke: A global history of smoking. London: Reaktion Books.

George Washington's Fredericksburg Foundation Fellows. (2000–2001). Tobacco and slavery in the Virginia Colony. History in your own backyard. Primers to the past: Teaching our history. Central Rappahannock Regional Library. Available from .

John B. Hutson Papers (#220), Special Collections Department, J. Y. Joyner Library, East Carolina University, Greenville, North Carolina.

Leavey, James. A history of tobacco. Available from .

Royal College of Physicians. (1962) Smoking and Health. Summary and Report of the Royal College of Physicians of London on smoking in relation to cancer of the lung and other diseases. New York: Pitman Publishing.

Shafey, O., Dolwick, S., & Guindon, G. E. (Eds). (2003). Tobacco control: Country profiles. Atlanta, GA: American Cancer Society. Available from .

U.S. Centers for Disease Control. (2007). Cigarette smoking among adults: United States, 2006. Morbidity and Mortality Weekly Report, 56(44), 1157–1161.

U.S. Centers for Disease Control. Cigarette use among high school students: United States, 1991–2005. Morbidity and Mortality Weekly Report, 200(55), 724–726.

U.S. Department of Health, Education and Welfare. (1964). Smoking and Health: Report of the Advisory Committee to the Surgeon General of the Public Health Service. Atlanta, GA: Public Health Service, Centers for Disease Control. Publication No. 1103.

U.S. Department of Health, Education and Welfare. (1967). Smoking and Health: The health consequences of smoking, a Public Health Service review. Atlanta, GA: Public Health Service, Centers for Disease Control. Publication No. 1696.

U.S. Department of Health, Education and Welfare. (1968). Smoking and Health: The health consequences of smoking: 1968 supplement to the 1967 Public Health Service review. Atlanta, GA: Public Health Service, Centers for Disease Control. Supplement to Publication No. 1696.

U.S. Department of Health, Education and Welfare. (1969). Smoking and Health: The Health Consequences of Smoking: 1969 supplement to the 1967 Public Health Service review. Atlanta, GA: Public Health Service, Centers for Disease Control. Publication No. 1696-2.

U.S. Department of Health and Human Services. (2004). The health consequences of smoking: A report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Page 101  |  Top of ArticlePrevention and Health Promotion, Office on Smoking and Health.

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.

World Health Organization. Tobacco use introduction for Japan. World Health Organization Infobase. Available from .

World Health Organization. (2008). Report on the global tobacco epidemic, 2008: The MPOWER package (p. 16). Geneva: Author.

Wynder, E. L., & Graham, E. A. (1950). Tobacco smoking as a possible etiologic factor in bronchogenic carcinoma. Journal of the American Medical Association, 143, 329–336.



The tobacco plant (Nicotiana tabacum) is native to the western hemisphere where it has grown from 6000 BC to 3000 BC and was used by indigenous peoples for religious and medicinal purposes. Since the seventeenth century, the cultivation and use of tobacco has spread worldwide. By the early twenty-first century, tobacco had become an industry worth $400 billion in annual revenues. Around one in three adults uses tobacco.


Tobacco, in its natural form, contains over three thousand compounds. Its cultivation, processing, and manufacture into various products; combination with other compounds; and routes of delivery; in turn, result in differences in absorption into the body. Tobacco smoke, for instance, contains over five thousand known chemical compounds, including highly volatile gaseous and vapor components and larger smoke particles (tar). There are at least fifty carcinogens released when a cigarette is smoked, including benzene, formaldehyde, and hydrogen cyanide. Some compounds increase the addictive properties of smoking, alter behavioral patterns, or produce additional effects in the brain and central nervous system (CNS).

The key substance found in tobacco is nicotine, a liquid alkaloid first isolated in 1828 by German chemists Wilhelm Heinrich Posselt and Ludwig Reimann. Nicotine makes up about 0.6 to three percent of dry weight of tobacco. It readily diffuses through the skin, lungs, and mucous membranes (such as the lining of the nose or gums), with the amount absorbed dependent on the type of tobacco leaf, method of use, and specific product. For example, cigarettes contain eight to twenty milligrams of nicotine, of which around one milligram is absorbed when smoked. Smokeless tobacco products (snuff and chewing tobacco) deliver three to four times the amount of nicotine delivered by a cigarette, which is absorbed more slowly but remains in the bloodstream longer.

The most common and expedient way to get nicotine into the bloodstream is through inhalation. Alveoli (tiny air sacs in the lungs where gas exchange occurs) provide an enormous surface area for access by nicotine. Once in the bloodstream, nicotine travels to the brain, taking an average of seven seconds. The nicotine then acts upon two nicotinic acetylcholine receptors in the brain—a ganglion type nicotinic receptor and a CNS type nicotinic receptor—increasing their activity. By binding to ganglion type nicotinic receptors, the adrenal medulla increases the flow of adrenaline (epinephrine), a stimulating hormone. This, in turn, causes an increase in heart rate, blood pressure, and respiration, as well as higher blood glucose levels. By binding to CNS type nicotinic receptors, dopamine levels in the reward circuits of the brain are increased, generating feelings of pleasure similar to that caused by cocaine and other stimulants. Other chemical messengers released by nicotine are acetylcholine, norepinephrine, vaso-pressin, arginine, and endorphins (small proteins that are often called the body's natural painkiller).

For the user, the amount of specific chemical messengers released, and the resultant feelings they induce, depend on the level of nicotine in the bloodstream. If a smoker takes short quick puffs on a cigarette, this will produce a low level of blood nicotine. Low doses enhance the actions of norepinephrine and dopamine in the brain, causing a stimulating effect that increases alertness and Page 102  |  Top of Articleconcentration. In contrast, deep puffs produce a high level of blood nicotine that enhances the effect of serotonin and opiate activity. This leads to an increase of acetylcholine and beta-endorphin, and a depression of the passage of nerve impulses. The result is a mild sedative effect, decreasing anxiety and producing a calming, even painkilling effect. Nicotine is thus unique in comparison to most drugs because its profile can change from stimulant to sedative/painkiller depending on dosage and use.

Nicotine has a half-life of one to two hours. The user must therefore self-dose with nicotine again to sustain its pharmacological effects. This repeated use is prompted by two further factors. First, tolerance develops over time so that users must absorb more nicotine to achieve the same effect, which explains how users can rapidly move to using increasing amounts of tobacco. Second, tobacco use leads to strong dependence or addiction. The pharmacological and behavioral characteristics that determine tobacco addiction are similar to those that determine addiction to such drugs as heroin and cocaine. While using nicotine-containing products, the body adapts the way it works to compensate for the effects of the nicotine. For example, neurons in the brain might increase or decrease the number of receptors or the amount of different neurotransmitters affected by the presence of nicotine. When there is no longer nicotine in the body, these physiological adaptations remain. The net result is that the body cannot function the same way in the absence of the drug as it did before, at least in the short term. Withdrawal symptoms include irritability, anxiety, depression and, above all, craving for nicotine. It is for this reason that, of the millions of people who try to stop smoking annually, only 10 percent succeed. In about a month, these feelings subside as physiological and psychological re-adaptation occurs.


Tobacco was first cultivated by the peoples of the pre-Columbian Americas, with large-scale cultivation beginning in the sixteenth century. In 1527 the first tobacco plantation was established in Haiti by the Spanish. In 1612 John Rolfe raised the first commercial crop of wild tobacco (Nicotiana rustica) in the English colony of Jamestown, Virginia, founded by Sir Walter Raleigh, for export to England. Growers soon switched to common tobacco(Nicotiana tabacum), a milder variety with rapidly growing demand in Europe. Within seven years, tobacco became the most valuable cash crop of the day, without which the American colonies would have failed. As tobacco farming expanded throughout the colonies, growers brought British prisoners, debtors, and eventually African slaves to work on the plantations.

In 1492 the South American Arawak tribe gave Christopher Columbus dried tobacco leaves, which he took back to Europe along with seeds. It was not until the mid-sixteenth century, however, that tobacco became popularized in Europe by sailors, explorers, and diplomats, such as Sir Frances Drake, Jean Nicot (after whom nicotine is named), and Francisco Herna´ndez de Toledo. By the 1600s, tobacco cultivation in Europe began to be established. Sir Walter Raleigh is attributed with establishing one of the first tobacco farms in England.

Tobacco was first introduced to the Middle East by the Turks who took it to Egypt in the early 1500s. It was introduced to China in the late 1500s via Japan and the Philippines, and in 1560 Portuguese and Spanish ships brought tobacco to East Africa where it then spread to Central and West Africa. Tobacco exports from South America to South Asia via Europe, through the British East India Trading Company and Dutch East Indies Company, commenced in the eighteenth century. This early trade arrived in eastern Mediterranean ports and was taken overland along the great Silk Road to Persia, Mughal, and China. The Portuguese colony of Goa was also supplied by sea. Under the Raj (1700–1800), widespread use of tobacco was established in South Asia, fuelled by an export drive by British merchants connected to the Virginian tobacco farmers. Initially smoked in pipes and hookahs, tobacco gradually became in-digenized, mixed with local spices and additives to produce such products as gutka. During the U.S. Revolutionary War in 1776, problems with supply led to large-scale tobacco farming in Africa and Asia by the 1800s. The glut in world production that resulted led to a decline in prices, making the hitherto luxury product more affordable, and thus fueling even greater demand.

In the early twenty-first century, tobacco was the world's most widely cultivated non-food crop, Page 103  |  Top of Articlecultivated in about 120 countries of diverse climates. It is favored by farmers because of its performance under widely varying climatic and soil conditions. The largest producers of tobacco leaf as of 2008 were China, the United States, India, Brazil, Turkey, Malawi, and Zimbabwe.


As tobacco has become a valuable commercial crop, techniques for growing and curing the leaf developed in sophistication. Different varieties of leaf are grown, varying in the growing conditions needed, taste (due to level of dextrose), and burning properties. Among the most popular are Virginia, Burley, and various Oriental tobaccos, with most products blending different leaf varieties. Once harvested, tobacco leaf is subject to various methods of processing. The most important is curing, which enhances the flavor of tobacco and increases its preservation by reducing the moisture level of the leaf. Initially leaf was naturally cured in the sun or by air, but artificial methods using fires or flues were used for larger-scale production. In 1839 it was discovered that flue-curing turns leaf grown on infertile sandy soil a bright yellow and orange color, thus establishing the lucrative brightleaf industry. Over time, various fuels to cure tobacco came to be used, including coal, oil, gas, and wood. There has been an ongoing search for more cost-effective and energy-efficient uses of oil and gas, alongside improvements in barn and furnace design, to reduce fuel requirements. In the early 2000s, many countries bulk-cure their tobacco in barns constructed out of metal that guarantee better pane insulation, more precise atmospheric control, reduced labor requirements, and more efficient energy use.

There are many ways that tobacco can be consumed. Smokeless tobacco products can be sniffed through the nose (powdered snuff), chewed, or dipped (placed between the cheek and gum). In Europe, snuff remained the most popular way of consuming tobacco until the nineteenth century. Chewing tobacco was also popular; in the United States, it was associated with cowboys from the nineteenth century, and in many parts of Asia, as part of everyday social life for men and women.

Smoking tobacco has been the main method of consumption since the late nineteenth century. Pipes were first used by North American Indians for medicinal and ceremonial purposes, and clay pipes became fashionable in Europe from the sixteenth century among both men and women. In East Asia, pipes were made of bamboo and sometimes ivory, whereas throughout the Ottoman Empire, men smoked waterpipes (also known as narghile, hookah, and shisha). The discovery of meerschaum (a soft white mineral) in the eighteenth century led to the production of fine quality carved pipes. For common use, wooden pipes progressively replaced fragile clay pipes, with briar burl becoming the material of choice.

The first cigars (from the Mayan word for smoking) originated in Cuba, which still produces the most sought-after cigars. Imported to Europe and the United States in the eighteenth century, cigars became popular among the wealthier classes. By the nineteenth century, smoking rooms began to be introduced on trains, and in private clubs and hotels, and the smoking jacket became fashionable. During the twentieth century, cigarillos (mini cigars) became a fast growing segment of the tobacco market, especially among cigarette smokers seeking to reduce the amount smoked, and by cigar smokers wanting to reduce costs.

The most common way of consuming tobacco since the late nineteenth century has been the cigarette. While early forms of cigarettes are believed to date from Central America in the ninth century, the rolling or stuffing of paper-wrapped cylinders with cured and finely cut tobacco leaves is attributed to Ottoman Turks around the 1830s. In 1843 the French tobacco monopoly began to manufacture cigarettes. In 1847 Philip Morris opened a shop in London selling hand-rolled Turkish cigarettes, switching to making his own in 1854. Because the process of hand rolling was slow (four cigarettes per minute) and labor intensive, cigarettes remained relatively expensive. The invention of the cigarette rolling machine in 1880 by James Bonsack, which could produce 12,000 cigarettes an hour, opened the way for mass production and consumption. James Buchanan Duke, later the first chairman of British American Tobacco (BAT), licensed the machine and by the late 1880s, the Duke Company was producing four million cigarettes per day. Alongside increased production, manufacturers developed new blends of tobacco leaf and Page 104  |  Top of Articleother ingredients, which gave specific brands a distinct flavor. One key ingredient was reconstituted tobacco which, given additives to make nicotine more volatile when burned, also made cigarettes more addictive.

In 2007, cigarette companies worldwide produced around 5.5 trillion cigarettes, representing around 96 percent of the world tobacco market. The top five consuming countries are China (1,643 billion), United States (451 billion), Japan (328 billion), Russia (258 billion) and Indonesia (215 billion). While the global cigarette market continues to grow, awareness of the harmful health effects of smoking has led to efforts to develop products of varying effect that seek to reduce harm, including the introduction of filters, lowering tar levels, nicotine replacement therapy (NRT), and smokeless products.


Efforts to control tobacco use largely date from the seventeenth century and initially focused on immorality and economic protectionism. Catholic and other spiritual leaders denounced the increasingly popular practice, some banning it from religious venues. King James I published A Counterblaste to Tobacco in 1604, introduced a 4,000 percent tobacco import tax to stem debauchery, and made imports a royal monopoly in 1614. In 1612 the Chinese emperor Kangxi passed an edict forbidding the planting and use of tobacco. Prohibition was introduced in Japan around 1620, and in Russia under the Romanoffs between 1613 and 1689. In 1683 Massachusetts and Pennsylvania forbid the smoking of tobacco outdoors for fear of fire. Various penalties were introduced, ranging from excommunication to execution.

The rapid growth in tobacco's popularity, and the lucrative profits generated, led to the repeal of most restrictions until the early twentieth century. In many countries, governments sought to exert monopoly control over production and trade, while the medical professions even claimed tobacco offered health benefits. The Lancet, for instance, stated that smoking cigarettes in moderation could help sufferers of tuberculosis. There remained limited opposition to tobacco use until the late 1800s when antismoking organizations began to form in Europe and the United States to encourage moderate use among adults. These organizations failed to attract mass support until the early 1900s when attention switched to smoking among children as a detriment to their physical fitness and morality. Legislation prohibiting the sale of tobacco products to children was first adopted at this time.

Health-based concerns about tobacco began to influence broader regulation from the 1930s onward. Statisticians for insurance companies began to link smoking to cancer and reduced life expectancy. German scientists, as part of the Third Reich's so-called Gesundheitspflicht (duty to be healthy) campaign, were among the first to link tobacco to lung cancer. By the end of the Second World War, alarming increases in morbidity and mortality from lung cancer brought more scientific and medical evidence to the fore. The work of Argentinian Angel Honorio Roffo showed that cancer all along the “smoking highway” (lips, tongue, throat, cheek, bronchial passages) was caused by exposure to tars released in the course of smoking (Proctor, 2006, p. 494). In Britain, Richard Doll and Austin Bradford Hill published their seminal paper in 1950 linking smoking to carcinoma of the lung. Ernst Wynder and E. A. Graham reported similar findings in the United States the same year. Over the next ten years, rapidly accumulating evidence of harmful health effects led to the publication of Smoking and Health by the Royal College of Physicians in 1962, and the Report of the U.S. Surgeon General in 1964.

By the 1980s, accumulated medical and scientific evidence showed smoking to be a known or probable cause of around twenty-five diseases, including various cancers, heart disease, and emphysema. Policy measures aimed at reducing demand by tobacco users, such as higher taxation, health warnings, and education, were widely introduced in established markets such as the United States and Europe. The health risks to nonsmokers (notably children, spouses, and coworkers) from secondhand smoke prompted measures to ban smoking in public places from the early 1990s. Other measures to regulate tobacco use included restrictions on marketing, advertising, and promotion; product design; and ingredients disclosure.

Throughout the second half of the twentieth century, public health advocates decried the pace and strength of regulation, weakened by the economic importance and political influence of the Page 105  |  Top of Articletobacco industry. The release of internal documents of the tobacco industry in the late 1990s revealed a well-organized and resourced campaign by the industry to undermine tobacco control efforts. The strategy included the funding of scientists to generate contrary evidence, lobbying of policy makers, and mobilizing of diverse allies to argue for the protection of civil liberties. The exposure of these tactics, along with data by the World Health Organization (WHO) attributing five million deaths annually to tobacco worldwide, led to growing support for stronger supply-side measures to control tobacco use. The adoption of the WHO Framework Convention on Tobacco Control (FCTC) in 2005 signalled recognition of the need for collective efforts across countries to strengthen both supply and demand side measures.


In 1527 Archbishop Bartolomé de Las Casas Cuzco of Spain is believed to be the first to write about tobacco's adverse effect on the brain, notably the inability of American Indians to stop smoking. However, nicotine addiction or dependence is a relatively recent concept whose definition has evolved over time. Prior to the 1920s, addiction was seen largely as a type of excessiveness, attributable by some to moral vice. From the late 1920s, research sought to find psychological correlates with the withdrawal of narcotic drugs, such as morphine, after prolonged use. This approach remained popular into the early 2000s, with addiction conceptualized as an uncontrollable disease and applied to the use of other substances, notably alcohol. A popular view of addiction in the 1960s, based on an assumption of physiological dependence by the user, refers to a state in which an individual needs to continue to take a drug in order to stave off unpleasant or dangerous withdrawal effects. The main shortcoming of this approach is that this motive plays a relatively modest role in the apparently unreasonable continued use of a drug. While many addicts experience withdrawal discomfort, this is only one aspect of a wider problem. Indeed, individuals attempting to stop using drugs, including nicotine, continue to relapse at a high rate long after withdrawal symptoms have resolved and controlling such symptoms may be insufficient to prevent relapse. Another outmoded definition of addiction is inclusion of the concept of intoxication. This view holds that addictive drugs lead to changes in users' psychological state, leaving some degree of impairment.

Since the late 1980s, generic criteria for defining substance dependence, such as those developed by the American Psychiatric Association and the WHO, focused on difficulties in controlling the use of the drug, of giving priority to drug use over other important obligations, to continued use of the drug in the knowledge of harmful consequences, and tolerance to the effects of the drug. While the criteria apply generically to substance abuse, they are seen as a suitable framework for determining the addictive or dependent nature of nicotine and smoking. On the basis of these criteria, the UK Royal College of Physicians concludes that “nicotine delivered through tobacco smoke should be regarded as an addictive drug, and tobacco use as the means of nicotine self-administration” (2000, p. 85). Nicotine replacement therapies have come to be accepted as part of the support needed by tobacco users seeking to stop.

See also Advertising and Tobacco Use; Britain: Tobacco Use and Policy.


Ferrence, R., Slade, J., Room, R. & Pope, M. (Eds.) (2000). Nicotine and public health. Washington, DC: American Public Health Association.

Gilman, S. L., & Zhou X. (Eds.). (2004). Smoke: A global history of smoking. London: Reaktion Books.

Goodman, J., Norton, M., & Parascandola M., (2005). Tobacco in history and culture: An encyclopedia. Farmington Hills, MI: Charles Scribner's Sons.

Kluger, R. (1996). Ashes to ashes. New York: Vintage Books.

Peele, S. (1990). Addiction as a cultural concept. Annals of the New York Academy of Sciences, 602, 206–220.

Proctor, R. N. (2006). Angel H. Roffo: The forgotten father of experimental tobacco carcinogenesis. Bulletin of the World Health Organization, 84(6), 494–496.

Royal College of Physicians. (2000). Nicotine addiction in Britain. London: Tobacco Advisory Group.

World Health Organization. (1964). Nomenclature and classification of drug- and alcohol-related problems: A WHO memorandum. Bulletin of the World Health Organization, 90, 225–242.



The tobacco industry is made up of the complex of primary suppliers, manufacturers, distributors Page 106  |  Top of Article(both wholesale and retail), advertising agencies, and media outlets that produce, promote, and sell tobacco products. It also includes the law, public relations, and lobbying firms that work to protect these products from stringent public-health regulation and control.

The industry evolved in the late nineteenth and early twentieth century from many relatively small enterprises that produced tobacco products for puffing, snuffing, and chewing. The products of these small firms delivered nicotine to the nasal and oral mucosa. With the evolution and refinement of the cigarette, the industry developed first into a monopoly and then into an oligopoly in which a handful of major producers made a more sophisticated nicotine delivery system: a device that delivers nicotine by inhalation to the lungs and thence rapidly to the brain. Although its popularity is declining in the United States, cigarette use is increasing worldwide at over 2 percent per year, especially in much of Asia, Eastern Europe, and the former Soviet Union. An integrated system of suppliers, manufacturers, marketers, and sales outlets is constantly evolving to supply this vast and growing market. In the past, sophisticated legal and lobbying enterprises managed to protect this industry from the sort of regulation advocated by a number of public health groups—regulations that governments routinely impose on far less toxic products—but an admonition from an internal source as to the effects of tobacco led to a dramatic increase of public and regulatory pressure on the tobacco industry.


Tobacco (nicotiana) is a plant of the nightshade family (genus Nicotiana) and is native to the Americas; it was a major commodity of commerce in colonial times. Cigar tobaccos were key exports from the Spanish and Portuguese colonies of the Caribbean and South America, while tobaccos for snuff, pipe, and chew were the economic mainstays of the English colonies in Virginia, Maryland, and the Carolinas. Whereas most of Europe (and the rest of the world) established state-run monopolies for tobacco distribution, private enterprise was the vehicle of tobacco commerce in Great Britain (and eventually in the United States). The state monopolies provided both a popular product for the populace and revenue for the national treasury—but private enterprise, which always paid excise tax in Great Britain, was more resourceful in expanding the market. This phenomenon was exploited in the twentieth century and was especially apparent in the 1990s, with the remaining state monopolies becoming privatized and adopting the marketing techniques of the by-now enormous transnational tobacco companies, often actually merging with them.


Relatively expensive, hand-rolled cigarettes became popular novelties in the United States and Europe in the mid-nineteenth century. The novelty came to dominate the industry over a period of forty years, from the mid-1880s to the mid-1920s, when, for the first time, more tobacco in the United States was used for cigarettes than for chewing tobacco.

A number of changes in the nineteenth century laid the groundwork for the cigarette's commercial success. The development of flue-cured tobacco and air-dried burley tobacco—easily processed into tobaccos for smoking (where the smoke might be inhaled) were major factors (Slade, 1993). Cigarette-making machines—first used commercially in 1883 by the American Tobacco Company—the development of safe matches, and an extensive railroad network to transport centrally manufactured cigarettes throughout the United States were among the other key factors responsible for this product's success.

Duke of Durham, North Carolina. These elements were successfully harnessed by Benjamin Newton (Buck) Duke, head of the American Tobacco Company. A working cigarette-making machine had been invented in 1881 by James Bonsack in response to a contest held by the cigarette maker Alan & Ginter of Richmond, Virginia (Smith, 1990). But the contest sponsors decided against using the invention since they did not know how to sell as many cigarettes as the machine was capable of making. Duke, however, realized that the low prices made possible by mass production, together with advertising to stimulate demand, would create a large enough market to absorb the vastly expanded production. He obtained favorable terms for using the machine in exchange for technical assistance in perfecting it. The machine Duke put on line in 1883 Page 107  |  Top of Articleproduced 120,000 cigarettes per day, the equivalent of 60 expert hand rollers. Duke's competitors had to pay more for Bonsack machines than he had, and Duke engaged in price wars to further weaken other manufacturers. Gradually, he bought out his competitors and monopolized the U.S. cigarette industry. By 1890, Duke controlled the cigarette market, and by 1910, just before his monopoly was broken, he controlled more than 80 percent of all tobacco products manufactured in the United States, except for cigars (Robert, 1952).

Seeking further growth, Duke began to expand his cigarette business overseas (Robert, 1952). By 1900, a third of the U.S. domestic production was being sent to Asia, and company factories were operating in Canada, Australia, Germany, and Japan. In 1901, Duke purchased a cigarette factory in Liverpool, England. Alarmed British manufacturers, seeking to avoid the fate of their U.S.compatriots, banded together as the Imperial Tobacco Company. The resulting trade war between American and Imperial ended in a truce. American was given exclusive trading rights in the United States and Cuba, and Great Britain became Imperial's exclusive territory. A new company, jointly controlled by both giants, was to sell cigarettes to the rest of the world. This modest sinecure was the birthright the parent companies gave the British-American Tobacco Company (BAT).

Antitrust Litigation. In 1907, the U.S. government filed an antitrust case against the American Tobacco Company. The result of this litigation was the dissolution of the trust four years later into a number of successor companies, some of which retain major roles in the U.S. cigarette market. These companies were the American Tobacco Company, the R. J. Reynolds Tobacco Company, Liggett & Myers, and P. Lorillard.

Once it had emerged from the confines of the trust, R. J. Reynolds, which had never before made cigarettes, developed and introduced Camel, a novel brand, in 1913 (Tilley, 1985). Camel was the first brand to combine air-dried burley, which had previously been important in chewing-tobacco products, with the then-conventional cigarette tobaccos—the flue-cured and Turkish (Oriental) varieties (Slade, 1993). Camel featured a coherent, national advertising campaign from N. W. Ayer that relied entirely on mass-media outlets in magazines and on billboards instead of on package-based promotions such as cigarette cards, coupons, and premiums. The legacy of this startling departure from the conventional cigarette-marketing techniques of the time is captured by the sly legend that still graces each pack of twenty unfiltered Camels sold in the United States: “Don't look for premiums or coupons, as the cost of the tobaccos blended in CAMEL Cigarettes prohibits the use of them.”

The other factor that distinguished Camel from its competitors was its price. While the leading brands of the time, such as Fatima, sold for fifteen cents per pack of twenty, a pack of Camel sold for a dime. In short order, Camel overwhelmed the competition and ushered in a dramatic expansion of the domestic cigarette market. American Tobacco copied the Camel formula with Lucky Strike, and Lig-gett & Myers followed with its copycat product Chesterfield. Cigarette cards, premiums, and coupons were abandoned in favor of the mass media, and prices fell. Cigarette use, then only rising slowly, began an unprecedented increase. This growth continued virtually unabated for forty years or so, until it finally slowed and eventually reversed by alarms that lung cancer and other major diseases could be caused by cigarettes (Fiore et al., 1993).

Only two firms that had no roots in the tobacco trust have played major roles in the U.S. cigarette market (Sobel, 1978). After Buck Duke's death in 1929, BAT purchased the Brown & Williamson Tobacco Company in Louisville, Kentucky. BAT gradually built this company into a major cigarette producer. For decades, its Kool brand dominated the menthol category, and during the 1930s and 1940s, its Wings brand gained market share by undercutting the prices of the majors. Brown & Williamson continues to offer a full range of cigarettes for the U.S. market in the early 2000s. It also produces cigarettes for export to many of BAT's international markets.

The other upstart company was Philip Morris, which began its U.S. operations as a specialty cigarette maker in New York in the first quarter of the twentieth century. In addition to its standard brand called Philip Morris, it produced Marlboro—a cigarette for “ladies.” The company expanded in the 1930s with a low-priced brand (Paul Jones) and a clever pricing scheme for Philip Morris English Blend (Robert, 1952; Sobel, 1978). It suggested Page 108  |  Top of Articlea retail price for the latter slightly above that for the major brands, but it gave retailers a larger margin, thus encouraging prominent display of the brand in stores. In the mid-1950s, Philip Morris gave Marlboro a filter and had the Leo Burnett advertising agency remake its image entirely to one of rugged masculine outdoor daring on horseback. (The entire sweep of Marlboro advertising is included in the special advertising collection of the American Museum of National History in Washington, D.C.) By the mid-1970s, Marlboro was the leading U.S. cigarette and by the 1990s, thanks to the strength of Marlboro's appeal to teens and young adults, Philip Morris overtook R. J. Reynolds to become the nation's largest tobacco-product manufacturer.

Smokeless Tobacco. Moist snuff and chewing tobacco enjoyed a 1980s and 1990s resurgence in popularity—this is based on the successful efforts of U.S. Tobacco (UST). It sells oral tobacco (e.g., Skoal Bandits, Skoal, Copenhagen) to adolescents and preadolescents (Denny, 1993). Oral tobacco is the only category of tobacco product whose consumption increased in the 1990s and early 2000s in the United States. This increase is attributable to UST's innovative marketing of moist snuff to adolescent boys and to imitation products from other manufacturers. Although UST envisions a global market for snuff, the World Health Organization has declared that countries in which oral tobacco is not a traditional product should ban it. A number of countries—including Australia, New Zealand, Hong Kong, and the European Community—have taken this step, often defying intense pressure from the U.S. government when doing so.


The tobacco industry adapts to changing circumstances in many ways. Product innovation is a key strategy. Since the early 1950s, the major changes in cigarette design have come in response to public-health concerns that cigarettes constitute a leading cause of illness and death (McGinnis, 1993; Slade, 1993). Most of these innovations have been variations on filters and so-called low-tar designs. Ballyhooed with multibillion-dollar advertising budgets, these innovations propped up cigarette consumption over the years despite the complete absence of demonstrated benefit at the time they were introduced. Years of study (and as many years of unregulated sale) have only produced evidence for decidedly marginal benefits, yet the innovations have become firmly established. These supposed advances have been criticized by some as being nothing more than public relations gimmicks in the face of and in mocking response to profound public-health problems.

The cigarette companies continue in the early twenty-first century to invent novel ways to deliver nicotine to the brain. Electronic devices, smokes with charcoal fuel elements, and tiny aerosol cans are but some of the gimmicks the companies have patented to facilitate the inhalation of nicotine. Despite these efforts, the industry remains dependent on smoking, with variations of the tobacco-filled cigarette the mainstay of its business for the foreseeable future.


Cigarette smoking has been declining in the United States, Canada, and Western Europe. Since the 1960s, however, the biggest cigarette manufacturers (BAT, Philip Morris, RJR/Nabisco, and, later, Japan Tobacco Incorporated) have steadily increased their business in international markets (Taylor, 1984). This expansion has been accompanied by the weakening and dissolution of both national private and state-owned tobacco companies. The process got under way in Latin America in the 1960s, spread to eastern Asia in the late 1980s, and developed into a frenzy of deal making in Eastern Europe and the republics of the former Soviet Union in the early 1990s (Shepherd, 1985; Sesser, 1993).

Shepherd has described the process whereby a transnational corporation moves toward dominating a formerly self-contained market through product innovation, smuggling, aggressive advertising, and pricing policies. The result is a larger market for tobacco products than existed previously and a corporate management that is better able to oppose public-health efforts at regulation and control. Although cigarette consumption is down in the United States, Canada, and Western Europe, it is rapidly growing in most of the world—especially the so-called third world. The transnational companies have positioned themselves to both fuel and profit from this trend. In an effort to reduce the public health impact from global expansion, the Page 109  |  Top of ArticleWorld Health Organization created the Framework Convention on Tobacco Control in 2007, giving support from wealthier nations to those in mid-low income nations to fight against tobacco company marketing efforts.


The giant cigarette makers have invested their tobacco profits in other enterprises for more than twenty years, ranging from soft drinks and cookies to office products, insurance, and real estate. This process has resulted in the ownership by tobacco companies of some widely known consumer-product companies, including Kraft and Nabisco. Although the parent tobacco companies pretend that this phenomenon makes them somehow less involved in tobacco (none now has the word “tobacco” in its corporate name), a thoughtful examination of these businesses reveals the following:

  • Tobacco products remain by far the most profitable sector of each of these conglomerates; and tobacco products are always responsible for most of the company profits.
  • Not one of these companies has backed away from any available opportunity to sell tobacco products. Indeed, the strongest companies continue to invest in domestic and overseas ventures that have as their goal the expansion of tobacco consumption.
  • These companies make ready use of nontobacco subsidiaries to support their tobacco businesses. For example, RJR/Nabisco fired the ad agency that did their Oreo Cookie advertising after that agency also produced ads promoting an airline offering smoke-free flights. Philip Morris has used one of its Kraft-General Foods warehouses for its coupon-redemption program for the Marlboro Adventure Team.

Tobacco companies do not diversify to get out of the tobacco business. They diversify because tobacco has given them profits, the acquisitions seem to be sound investments, and the resulting product mix complements the core business in some manner.


Price competition has long been part of the tobacco industry strategy. It was the major tool for the achievement of monopoly power in the 1880s and was a key element in the early twentieth-century dominance of the market by Camel. In the 1930s, price competition, made possible by overly aggressive price increases by the majors, contributed to the emergence and growth of Brown & Williamson and Philip Morris (Sobel, 1978). From the end of World War II (1945) until 1980, however, price competition was virtually absent from the U.S. cigarette market.

In 1980, tiny Liggett & Myers, a firm that had become too small to enjoy oligopolistic profits, broke ranks with its fellows by introducing generic cigarettes. The strategy was made possible by the pattern of price increases in the industry—increases that had exceeded the rate of inflation for years. Brown & Williamson soon followed suit with its own generic brands, and within a few years every cigarette manufacturer had a multitiered pricing structure, with the heavily advertised, standard brands at the top. Prices for the major brands continued to rise steeply, far faster than inflation, through early 1993. Customers who might have stopped smoking because of high prices were kept in the market by the increasingly available lower priced offerings. By early 1993, however, investment analysts had become concerned because lower priced brands accounted for more than 25 percent of all cigarette purchases—with attendant threats to profits—and Philip Morris had become alarmed by the market share losses sustained by its cash cow, Marlboro, to less than 25 percent of all cigarettes sold.

Philip Morris had a number of key strengths that gave it a flexibility not possessed by its competitors, including market leadership, an absence of corporate debt, and a strong youth market for Marlboro. Its principal competitor, RJR/Nabisco, had an enormous corporate debt—and although Camel had been making inroads into Marlboro's youth market, it was still far from the dominant cigarette. These factors led Philip Morris to cut prices substantially (while mounting the most elaborate promotional campaign ever seen in the industry). The competition was forced to follow suit with lower prices. Marlboro's brand share surged; the threat to profitability from lower priced brands subsided; and the competition was left somewhat weakened.


In 1915, the U.S. tobacco industry formed the Tobacco Merchants Association (TMA) to lobby Page 110  |  Top of Articleagainst the anticigarette laws that had become a problem for the industry in a number of states (Robert, 1952). These laws came about as a result of the efforts of antitobacco advocates, including Henry Ford and Thomas Edison. The TMA accomplished its objectives: By 1930, the state prohibitions on cigarettes had been diminished to easily ignored prohibitions that only barred the sale of cigarettes to minors.

In the 1950s, the industry faced a more substantial challenge—proof that cigarettes caused lung cancer. In addition to putting cosmetic filters on the product and making outrageous claims for their benefit (P. Lorillard trumpeted its asbestos-filtered Kent as “the greatest health protection in cigarette history”), the industry developed a sophisticated public relations and lobbying capability (Wagner, 1971). The public relations firm of Hill & Knowlton organized the Tobacco Institute to meet the industry's public relations and lobbying needs. The cigarette makers also formed the Tobacco Industry Research Committee (later reorganized and renamed the Council for Tobacco Research) to create the pretense that the industry was conscientiously involved in biomedical research to get to the bottom of the smoking and health question (Freedman & Cohen, 1993).

Although speculation existed as to how diligently the tobacco industry would pursue smoking research, they did in fact do so, but their conclusions, giving more light to the fact that tobacco is addictive and harmful, were not released. Routinely called the tobacco cover-up it resurfaced in later years with much of its strength coming from Bennett S. LeBow's agreeing, in 1997, to put warnings on cigarette packs stating that smoking is addictive. Leaked internal documents also served as evidence of the dangers. In 1998, however, other tobacco companies still contested that tobacco was not an addictive drug. Discovery, through LeBow, of the industry's nondisclosure and the understanding that the industry had evidence of the threat of smoking, however, caused severe public attacks on the tobacco industry to be more common. Public campaigns have also been more potent with reducing youth smoking. Between 1998 and 2000 smoking had declined 54 percent in middle schools and 25.2 percent in high schools. Then, too, tobacco advertising legislation has weakened the strength of tobacco propaganda

Table 1. Leading U.S. tobacco companies. Major tobacco-product manufacturers in the United States, the location of their corporate headquarters, and the major tobacco brands they market.
Company Home office Major brands
Phillip Morris (Altria) Richmond, VA Marlboro
Benson & Hedges
Virginia Slims
RJ Reynolds (Nabisco) Winston-Salem, NC Camel
Pall Mall
Natural American Spirit
Lorrillard (Loew's Corp) Greensboro, NC Kent
Moist snuff
UST Stamford, CT Copenhagen
Skoal Bandits
Skoal Classic

Table 1. Leading U.S. tobacco companies. Major tobacco-product manufacturers in the United States, the location of their corporate headquarters, and the major tobacco brands they market. Table 1. Leading U.S. tobacco companies. Major tobacco-product manufacturers in the United States, the location of their corporate headquarters, and the major tobacco brands they market. ILLUSTRATION BY GGS INFORMATION SERVICES. GALE, CENGAGE LEARNING

among youth populations by banning all advertising that is determined to be too appealing to a minor.

As of 2008 more legislation was being proposed and being worked on to make nicotine a drug regulated by the FDA. Previously, the FDA has tried to apply regulations to tobacco and cigarettes as a nicotine delivery agent, but the courts had determined that Congress had not yet given the regulatory administration such authority, so new legislation must be passed for successful and lawful regulation. If such a bill is passed tighter control will be possible so that tobacco can be prohibited at public events where minors may be part of the targeted demographic, in response to public outcry. Furthermore, tobacco companies are prohibited from sponsoring public events and athletic competitions. In some states, legislation has also already been passed, and tried, winning large cash settlements to recover lost health costs suspected to be tobacco-use related. Included in some of these settlements have also been requirements for the tobacco companies to pay for more advertisements intended to reduce youth smoking. Despite the research, such as it was, the mounting costs to the tobacco companies because of law suits and penalties, and in the face of growing evidence of harm from a variety of other Page 111  |  Top of Articlequarters, the smoking epidemic continues into the early twenty-first century.

The Tobacco Institute, in alliance with the various branches of the industry, stood as a bulwark against public-health activities for a generation. After the Master Settlement Agreement in 1998, the Tobacco Institute was reduced to a Web site of searchable documents directly related to tobacco industry lawsuits. The Council for Tobacco Research has funded studies of marginal importance for public relations gain while operating a Special Projects branch for the benefit of tobacco-product liability defense. In these and other ways, the tobacco industry has attempted to insulate itself from significant regulation and from acceptance of any responsibility for the harm its products cause. Similar organizations exist to protect the interests of oral-tobacco manufacturers.


The major tobacco-product manufacturers are publicly owned and traded corporations. As such, they are owned by their investors. Major institutions, including banks, insurance companies, and pension funds, hold the majority of shares in the tobacco industry.

The tobacco industry is a powerful oligopoly of product manufacturers in alliance with a network of suppliers and associated service organizations. Although its products form the leading cause of preventable death, it continues despite public sentiment and attempts to protect itself against appropriate regulation by extensive legal, public relations, and lobbying efforts. The industry is understandably driven by an interest in making money. It has never acted out of a primary concern for the health of its customers or the health of those around them. For a variety of reasons, including clever intervention by the industry, government has utterly failed to provide the sort of regulatory control expected when it comes to something as addicting and toxic as nicotine-containing tobacco products until a critical documentation leak occurred from within the companies of the tobacco industry.

See also Advertising and Tobacco Use; Nicotine.


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As of 2006, there were about 45 million cigarette smokers in the United States, representing 21 percent of the adult population. Another 2 percent were cigar smokers, and 2 percent used smokeless tobacco (chewing tobacco or snuff) (Morbidity and Mortality Weekly Report, 2007). More than half of tobacco users are dependent on (addicted to) nicotine, an alkaloid that is the main psychoactive ingredient in tobacco. Most of them will have to try to quit several times before they are successful. Both the direct effects of nicotine on the body and behavioral associations with those effects learned over the years of tobacco use keep people smoking even when they want to quit.

The role of nicotine in tobacco use is complex. Nicotine acts on the body directly to produce effects such as pleasure, arousal, enhanced vigilance, relief of anxiety, reduced hunger, and body-weight reduction. Nicotine (whether in tobacco or nicotine-containing medications) can reverse the withdrawal symptoms that occur in a nicotine-dependent person trying to quit, when nicotine levels in the body fall. These symptoms include anxiety, irritability, difficulty concentrating, restlessness, hunger, depression, sleep disturbance, and craving for tobacco. Nicotine also acts indirectly, through a learning process that occurs when the direct effects of nicotine occur repeatedly in the presence of certain features of the environment. As a result of this learning process, called conditioning, formerly insignificant environmental factors become cues for the direct actions of nicotine. These factors can become pleasurable in themselves or they can serve as a triggering mechanism for lighting up a cigarette. For example, the taste, smell, and feel of tobacco often evoke a neutral response and sometimes repugnance in a nonsmoker. After years of experiencing the direct effects of nicotine in the presence of tobacco, however, a smoker finds the sensory aspects of tobacco pleasurable.

The indirect or conditioned effects of nicotine can be responsible for much more complicated learning than the learning associated with nicotine's direct effects. Conditioning is also the process whereby the situations in which people often smoke, such as after a meal, with a cup of coffee, with an alcoholic beverage, while doing a task at work, while talking on the telephone, or with friends who also smoke, become in themselves powerful cues for the urge to smoke. When people stop using tobacco, therefore, the direct effects of nicotine are not the only pleasures they must give up. They must also learn to forgo the indirect effects of nicotine: those experiences that, through learning, have become either pleasurable in themselves or a cue to smoke.


Many nicotine dependent smokers want to quit smoking; however, once dependence on nicotine or tobacco is established, cessation becomes difficult. The reasons for wanting to quit vary. The most common include (1) a concern for one's health, (2) a concern for the health of family members and others due to the harmful effects of secondhand smoke, (3) social pressure exemplified in laws by state or municipal governments prohibiting smoking in certain indoor locations (such as restaurants and bars) and outdoor environments (such as in areas within the vicinity of hospitals or schools); and (4) economic factors (cigarettes have become increasingly expensive).

Successful quitting of tobacco use usually occurs through a series of mental stages or steps (Prochaska & DiClemente, 1983): (1) Precontemplation: the smoker has no intention to stop smoking during this stage; (2) Contemplation: the person is thinking of quitting but not within the next six months; (3) Action: the smoker has a stop date and a plan that is or will be implemented within one month; (4) Maintenance: the person has discontinued the regular, daily use of tobacco for a minimum of one month. Most regular tobacco users go through these stages of change several Page 113  |  Top of Articletimes before they are successful. Although developed in relation to smoking cessation, these stages of change have been applied to the process of stopping other addictive behaviors.


Relapse is a cardinal feature of substance dependencies, including nicotine dependence. To paraphrase Mark Twain: Quitting smoking is easy, I've done it a thousand times. Most quit attempts that are successful in the short-term are followed by a return to smoking or other tobacco use within a few weeks, sometimes days, of stopping. For example, 66 percent of smokers who try to quit on their own or with minimal outside help relapse within two days, 90 percent relapse within three months, and 95 to 97 percent relapse within one year of quitting. The key to successful smoking cessation is an understanding of the particular triggers that provoke relapse and the strategies that are effective in preventing relapse. Withdrawal symptoms, which can begin within hours of the last use of tobacco, are important triggers for cravings to smoke again. Emotional reactions to stress, such as depression and anxiety, and environmental cues that have acquired an association with smoking can also serve as powerful triggers of urges to smoke.


To avoid succumbing to urges to smoke, former tobacco users must develop ways of coping with and managing triggers for smoking. Shortly after quitting, when the strength of withdrawal symptoms and environmental cues is greatest, behavioral techniques such as the following are helpful: (1) removing ashtrays from one's home and office, (2) leaving the table as soon as possible after meals and engaging in other activities such as talking, walking, or doing the dishes; (3) avoiding (at least temporarily) situations that used to occur with smoking, such as drinking alcohol, coffee, or other beverages linked with smoking; (4) avoiding situations in which other smokers are likely to be around, and (5) actively seeking social support for smoking cessation. The encouragement of a spouse, family members, or friends who are nonsmokers or who are in the process of quitting, can make it easier to avoiding lighting up again. Smokers who enjoy having something in their mouths or handling cigarettes can substitute something for these smoking-related tactile behaviors. They can chew gum, toothpicks, or sunflower seeds; munch low-calorie snacks; and snap, roll, or twist rubber bands on their wrist. What people think about while quitting is also an important factor for preventing relapse. Instead of thinking about the expected pleasures of a cigarette, the would-be quitter can substitute thoughts about the health hazards of smoking, the health benefits of not smoking, or the pleasures of an anticipated reward for not smoking.

These urges to smoke, or cravings, can re-occur long after the nicotine withdrawal period has ended, usually provoked by conditioned cues to smoking, frequently the onset of strong emotional events formerly managed by smoking. Applying the strategies learned during the weeks shortly after quitting can help the former smoker to overcome temptations to smoke that challenge one's ability to maintain abstinence in the long term.


Most efforts to quit occur without professional help. Persistence in avoiding a return to smoking is essential; most smokers try to quit several times before they are successful. Many aids are available to tobacco users who quit on their own. Smoking-cessation program guides and motivational and educational audiotapes and videotapes are obtainable from physicians, hospitals, or organizations such as the American Lung Association, the American Cancer Society, or the American Heart Association, or they may be found in bookstores and libraries.


Smoking-Cessation Programs. Resources for smokers who seek help for quitting are available in most communities in the United States. Smoking cessation clinics can be found in most hospitals and community health centers. Information regarding the location and availability of smoking cessation programs can be obtained from a nationally based telephone resource at 1-800-QUIT-NOW (1-800-784-8669).

Physician- and Clinic-Assisted Quitting. Physicians' offices and hospital clinics that offer Page 114  |  Top of Articlesmoking cessation assistance are particularly useful for people who have medical problems, for people who have tried before and failed to quit, or for people who may benefit from smoking cessation medications. Smokers can turn to these health-care facilities for advice on how to quit, for self-help material, for support and information about other cessation resources that could be more suited to their needs, and if necessary, prescriptions for medications to ease the difficulties of withdrawal and increase their chance of successfully quitting.

Pharmacotherapies for Tobacco Dependence. Smokers who have tried to stop smoking on their own but failed are candidates for treatments with smoking cessation medications. First-line medications approved as cessation aids by the U.S. Food and Drug Administration (FDA) include the various nicotine replacement systems, such as nicotine chewing gum, nicotine patch, nicotine nasal spray, nicotine inhaler, and nicotine lozenge; and two non-nicotine medications, bupropion (Zyban) and varenicline (Chantix). Second-line medications, which are not FDA-approved for this indication, include nortriptyline and clonidine, and combination pharmacotherapy (United States Department of Health Human Services, 2008).


The nicotine replacement therapies (NRT) when used as directed all approximately double the likelihood that a person will successfully quit smoking. NRT can reduce the severity of nicotine withdrawal. Research has suggested that prolonged use of these medications can extend the period of abstinence. Some tobacco users are concerned about the hazards of nicotine, but the hazards of NRT are much less than those associated with smoking. First, the amount of nicotine ingested through the replacement therapies is less than that taken in from cigarettes. Second, nicotine-replacement medications do not expose smokers to the other hazards of cigarette smoke, which include carbon monoxide, tar, cyanide, and a number of other toxic substances. On balance, using the nicotine replacement systems is much safer than smoking cigarettes. The nicotine-replacement medications are particularly useful with more seriously addicted smokers, but they are not a simple cure; rather, they should be used as part of a program of learning to live a tobacco-free lifestyle.

Nicotine Chewing Gum. The chewing gum is available without a prescription and comes in strengths of 2 and 4 milligrams (mg), although the dose actually delivered to the chewer is 1 mg and 2 mg, respectively. The 4-mg formulation has greater utility for heavier smokers (those smoking more than twenty cigarettes daily). Nicotine is absorbed from the gum gradually over twenty to thirty minutes, in the course of which blood nicotine levels are similar to those seen after smoking a cigarette. The gum should be chewed intermittently, to allow time for the nicotine in the saliva to be absorbed. Nicotine gum should be chewed regularly throughout the day, and when urges to smoke are felt. For maximum benefit, nicotine gum should not be chewed within ten minutes of drinking any beverage because certain beverages such as coffee, fruit juice, or cola drinks reduce the absorption of nicotine. Most people need to chew eight to ten pieces per day to obtain optimal benefits, usually for three to six months, but fewer pieces can be used during the later period of nicotine gum use. Side effects from chewing nicotine gum may include fatigue and soreness of the jaw, loosening of dental fillings, and occasionally nausea, indigestion, gas, or hiccups, particularly if one has chewed the gum so rapidly as to swallow nicotine-rich saliva.

Nicotine Patches. This formulation of nicotine treatment is also available as an over-the-counter medication. Patches deliver nicotine in its un-ionized (uncharged) chemical form, thereby allowing the drug to pass through the skin readily. Various patches deliver different doses and are applied to the skin once a day for periods that range from sixteen to twenty-four hours within the day. The higher dose patches (usually 21 mg) are used during the initial four weeks of quitting, and lower-dose patches (14 mg and 7 mg) are available for subsequent tapering. A single-dose nicotine patch (15 mg) used for sixteen hours during the day, which is recommended for eight weeks' use, is also available. Smokers who want to quit are instructed to first stop smoking and then to apply the patch daily, usually upon waking up. Side effects from nicotine patches may include itching or burning over the patch site, which usually subsides within an hour, and local redness and mild swelling. Some people experience a sense of stimulation, and occasionally, insomnia and vivid dreams. These effects tend to occur during the Page 115  |  Top of Articlefirst few days of patch use but diminish with longer patch use. There was initial concern regarding the cardiovascular safety of smoking while using the patch, though this has not been borne out. Nicotine patch users who are unable to resist one or two cigarettes are much better off keeping the patch on, to prevent a full-blown return to smoking, rather than removing the patch.

Nicotine Lozenge. The nicotine lozenge, like the nicotine gum, is an oral form of nicotine replacement and is also available as an over-the-counter medication. The nicotine lozenge comes in the form of hard candy, and should be dissolved in the mouth rather than chewed or swallowed. Patients are advised to use one lozenge every one to two hours, or a minimum of nine lozenges per day for the first six weeks, then to reduce to one lozenge every two to four hours during the seventh to the ninth week, and one lozenge every four to eight hours for weeks ten to twelve. Use beyond twelve weeks is not recommended. Patients should not drink or eat immediately before using the lozenge or while it is in the mouth. The most common side effects from nicotine lozenge are nausea, hiccups, heartburn, coughing, and headache. More nicotine is delivered through the lozenge than the gum because the lozenge dissolves completely whereas a residual amount of nicotine is retained in the gum. A comparison of safety profiles showed similar tolerability of the nicotine lozenge and the nicotine chewing gum.

Nicotine Inhaler. The nicotine inhaler consists of a plastic tubelike mouthpiece into which is placed a cartridge containing a nicotine-impregnated plug. Nicotine vapor is produced when warm inhaled air passes through the plug and nicotine is delivered through the buccal mucosa. The inhaler produces a rate of nicotine delivery similar to the nicotine gum. Eating and drinking acidic beverages such as coffee and juice should be avoided fifteen minutes before or after use of the inhaler. Dose is related to temperature; low temperatures will inhibit the release of nicotine. Use of the inhaler for up to six months with gradual reduction in frequency during the last two months is recommended. Clinical trials of the nicotine inhaler have shown that it doubles quit rates obtained with placebo, similar to the effects observed with the other nicotine replacement systems. Side effects from the inhaler include mild irritation of the mouth and throat, coughing, and runny nose. The frequency and severity of these symptoms decline with continued use of the inhaler.

Nicotine Nasal Spray. The nicotine nasal spray was designed as a more rapid means of delivering nicotine to the smoker than the gum or the patch. The nasal spray consists of a small bottle containing a 10-mg/ml nicotine solution. A 50-milliliter spray containing 0.5 mg nicotine can be conveniently delivered using an accompanying manual pump. Each dose consists of two squirts, one to each nostril. This mechanism can deliver nicotine to the brain within ten minutes, providing the most rapid nicotine delivery among the currently available nicotine replacement delivery systems. Patients are advised to use one or two doses per hour and may increase as needed. The minimum treatment is eight doses per day, with a maximum limit of forty doses per day or five doses per hour. The recommended duration of therapy is three to six months. The nicotine nasal spray has some potential to produce dependence manifested either in increased frequency of use or in longer duration of use than recommended, associated with its greater rapidity in producing nicotine effects compared to the other forms of NRT. The side effects associated with the nasal spray are irritation of the nose and throat, sneezing, coughing, and teary eyes. These symptoms often occur during the first week of use but typically decline with continued use.

Bupropion. Bupropion sustained release (SR) is a non-nicotine medication that is available by prescription only. Bupropion was originally marketed as an antidepressant (Wellbutrin). On the strength of evidence from several placebo-controlled trials, the FDA approved the marketing of bupropion (SR), under the trade name Zyban, as a treatment aid for smoking cessation. The mechanism by which bupropion assists smokers is not clear but it is thought to be related to both noradrenergic and dopaminergic activity in the brain. Patients are advised to begin using bupropion at a dosage of 150 mg per day for three days, then to increase to 150 mg twice a day for one to two weeks prior to a selected quit date, with continued treatment Page 116  |  Top of Articlefor seven to twelve weeks following the quit date. Bupropion has been shown to reduce withdrawal symptoms and to reduce the weight gain usually associated with stopping smoking. The most common side effects reported by bupropion users have been insomnia and dry mouth. Bupropion is contraindicated in persons with a history of seizures, or of eating disorders, and those who have used a monoamine oxidase inhibitor in the past fourteen days. Recent research has suggested that extending bupropion use beyond eight to twelve weeks can increase the period of abstinence, although the risk of smoking again appears to return once the medication is no longer used (Covey et al., 2007).

Varenicline. Varenicline was approved by the FDA under the trade name Chantix as a treatment for nicotine dependence. The development of vare-nicline for smoking cessation was based on knowledge regarding the pharmacology of nicotine addiction, specifically the role of acetylcholine-receptor subtypes in the mediation of nicotine addiction. Through high affinity and high selectivity at the alpha4beta2 nicotinic acetylcholine receptor site, var-enicline exerts agonist effects—reducing withdrawal symptoms, and antagonizing the effects of ingested nicotine—limiting the reward and pleasure associated with smoking. Industry-sponsored trials of var-enicline, conducted among healthy smokers aged eighteen years or more who smoked at least ten cigarettes daily, showed that compared to placebo treatment, varenicline more than doubled the abstinence rate at the end of twelve weeks of treatment and at fifty-two weeks after the initial quit date (Lam & Patel, 2007). In addition, head-to-head trials showed higher abstinence rates at the end of twelve-week treatments and one year after quitting with varenicline compared to bupropion. A maintenance treatment trial showed that extending the treatment period by another twelve weeks modestly increased the abstinence rate, although the protective effect of varenicline seemed to abate upon discontinuing its use. The recommended dosing regimen is 0.5 mg once daily for the first three days, then 0.5 mg twice daily for days four to seven, and 1 mg twice daily to complete twelve weeks of treatment. Mild-to-moderate nausea was the most commonly reported side effect (about 30 percent of trial participants); other adverse events reported by more than 10 percent of study participants were headache, insomnia, and abnormal dreams.

Unlike bupropion, which had been available for several years as an antidepressant medication, the post-marketing information about the side effects of varenicline has been limited. Concerns have been raised regarding possible adverse reactions among smokers with comorbid psychiatric conditions, for example, schizophrenia and bipolar disorder, who were excluded in the pivotal clinical trials; further research to determine varenicline's safety and efficacy among such populations is needed.


Clonidine (Catapres) is an alpha2-noradrenergic agonist that was initially used for the treatment of hypertension, and subsequently found to diminish symptoms of both opiate and alcohol withdrawal. The efficacy of clonidine as a short-term smoking cessation aid was demonstrated in several studies in which clonidine was delivered either orally or in patch form. This drug has not received FDA approval as a smoking cessation aid, however, and should be considered to be a second-line treatment to be used when first-line pharmacotherapies have not been successful. Clonidine use is associated with reductions in pulse rate and blood pressure, and abrupt discontinuation could result in a rapid rise in blood pressure and catecholamine levels. Side effects reported with clonidine use include dry mouth, drowsiness, dizziness, and sedation. Appropriate dosage levels have not been established as of 2008.

Nortriptyline is used primarily as an antidepressant (Pamelor). Results from several trials of nortriptyline as a smoking cessation aid have found that it can double the abstinence rate at the end of treatment, similar to the effect of bupropion. Nortriptyline has not been approved by the FDA for the treatment of tobacco dependence, mainly because of a more complicated side effect profile than the first-line medications (including cardiovascular changes), and the small number of trials that have evaluated nortriptyline for smoking cessation. In the smoking cessation trials, nortriptyline use was initiated at a dosage of 25 mg/day, and increased gradually to 75 to 100 mg per day over twelve weeks. Sedation, dry mouth, blurred vision, Page 117  |  Top of Articleurinary retention, lightheadedness, and shaky hands are the most commonly reported side effects of nortriptyline use.

Other Treatments. A number of other treatments have been used to aid in smoking cessation: hypnosis, acupuncture, lobeline and silver acetate medications. The effectiveness of these treatments has not been established by medical research, although some individuals may benefit from them. None of these treatments, however, can cure smokers of their tobacco addiction without the commitment and effort that are usually required to quit.

Combination Pharmacotherapies. Evidence from multiple published studies support the effectiveness of several types of combination treatments; these include nicotine patch + bupropion, nicotine patch + nicotine inhaler, long-term nicotine patch use (eighteen to twenty-four weeks) + ad libitum nicotine gum or nasal spray, nicotine patch + nor-tripyline, and nicotine patch + antidepressants (paroxetine and venlafaxine). All of these combination treatments significantly increased abstinence at the end of treatment and at twelve months follow-up. Individual patient characteristics, for example, depressed mood at the time of making the cessation attempt, and patient preference are useful indicators for selecting the appropriate type of combination treatment.


There has been increasing recognition that tobacco use and nicotine dependence are more prevalent among individuals with psychiatric illness and substance use (alcohol or drugs) disorders. Persons with mental disorders comprise 20 percent of the population yet consume 44 percent of cigarettes and tobacco in the United States. The prevalence of nicotine dependence in the general population is about 13 percent but significantly higher among persons with mental illness or alcohol and substance use (other than nicotine) disorders (Grant et al., 2004). Several explanations for the high comorbidity of psychiatric illnesses and nicotine dependence have been considered: (1) because nicotine can affect brain structure, tobacco use, which typically starts during adolescence, can cause susceptibility to mental illness and drug dependence; (2) because nicotine exerts positive effects on mood as well as reduces psychiatric symptoms, nicotine could be used for self-medication; and, (3) common factors, such as genetics or shared environment, account for the susceptibility to nicotine dependence and mental illnesses. Empirical support for these mechanisms has been reported, making it possible that any single one of them or combinations thereof are applicable in individual cases where tobacco dependence and psychiatric conditions co-occur.

Although it is clear that there is a higher prevalence of tobacco use among mentally ill and drug dependent populations, the likelihood as well as the consequences of smoking cessation when psychiatric illness is present remain controversial. Epi-demiological evidence has tended to show lower smoking cessation rates among persons with affective and anxiety disorders as well as persons with current alcohol and drug disorders, but contrary evidence has also been reported. Findings from clinical trials of smokers have also been mixed. It is possible that variation in severity or treatment of the comorbid disorder affects the likelihood of successful cessation. For example, a meta-analysis showed that among individuals who receive active treatments, for example, clonidine, bupropion, nortriptyline, or nicotine replacement therapy, or cognitive therapy for mood management, smokers stopped smoking at similar rates irrespective of whether they had a past history of major depression. However, among individuals who did not receive an active treatment (for example, those treated with placebo), a lower smoking cessation rate was observed among those with past major depression, particularly, the more severe, recurrent type of major depressive disorder (Covey, Bomback, & Yan, 2006).

Another clinically important but unresolved issue is the effect of smoking cessation on recurrence of mental illness or substance use relapse. Although more work remains to be done and exceptions have occurred, studies of persons with past major depression and schizophrenia have suggested that smoking cessation can occur without risk of exacerbating symptoms of the comorbid psychiatric condition (Hall, 2007). Studies of smokers with substance dependencies have also produced mixed results. A meta-analysis of nineteen trials of smokers who were either in treatment or recovering from substance dependence found Page 118  |  Top of Articlethat smoking cessation treatment enhanced rather than impeded long-term sobriety (Prochaska, Delucchi, & Hall, 2004). Further studies of this important question are needed; however, a well-controlled trial of 499 persons receiving treatment for alcohol dependence showed that concurrent smoking cessation treatment resulted in higher rates of alcohol relapse compared to delayed smoking cessation treatment (Joseph et al., 2004).

Many persons who are dependent on tobacco want to quit but multiple barriers to tobacco cessation treatment remain. These include lack of knowledge about the availability of efficacious treatments, and lack of confidence on the part of smokers and health practitioners that tobacco cessation efforts will be successful. Removing these barriers are challenges to the public health and medical community. A significant barrier as well is the perception that cessation treatments are too expensive. In fact, tobacco cessation is one of the most cost-effective health interventions (Croghan et al., 1997) and, through its effect on reducing the morbidity and mortality of tobacco-related diseases, has the most far-ranging effects of any medical service in improving longevity and the overall quality of life (National Cancer Institute, 1997).

See also Addiction: Concepts and Definitions; Nicotine; Nicotine Delivery Systems for Smoking Cessation; Treatment, Stages/Phases of: Relapse Prevention; Withdrawal: Nicotine (Tobacco).


Covey, L. S., Bomback, A., & Yan, G. W. (2006). History of depression and smoking cessation: A rejoinder. Nicotine and Tobacco Research, 8(2), 315–319.

Covey, L. S., Glassman, A. H., Jiang, H., Fried, J., Mas-mela, J., Loduca, C., et al. (2007). A randomized trial of bupropion and/or nicotine gum as maintenance treatment for preventing smoking relapse. Addiction, 102(8), 1292–1302.

Croghan, I. T., Offord, K. P., Evans, R. W., Schmidt, S., Gomez-Dahl, L. C., Schroeder, D. R., et al. (1997). Cost-effectiveness of treating nicotine dependence: The Mayo Clinic experience. Mayo Clinic Proceedings, 72(10), 917–24.

Grant, B. F., Hasin, D. S., Chou, S. P., Stinson, F. S., & Dawson, D. A. (2004). Nicotine dependence and psychiatric disorders in the United States: Results from the national epidemiologic survey on alcohol and related conditions. Archives of General Psychiatry, 61(11), 1107–1115.

Hall, S. M. (2007). Nicotine interventions with comorbid populations. American Journal of Preventive Medicine, 33(6), Suppl 1, S406-S413.

Joseph, A. M., Willenbring, M. L., Nugent, S. M., & Nelson, D. B. (2004). A randomized trial of concurrent versus delayed smoking intervention for patients in alcohol dependence treatment. Journal of Studies on Alcohol, 65(6), 681–691.

Lam, S., & Patel, P. N. (2007). Varenicline: a selective alpha4beta2 nicotinic acetylcholine receptor partial agonist approved for smoking cessation. Cardiology Review, 15(3), 154–161.

Morbidity and Mortality Weekly Report. (2007, November 9). 56(54), 1157–1161.

National Cancer Institute. (1997). Changes in cigarette-related disease risks and their implication for prevention and control. NIH Publication No. 97-4213.

Prochaska, J. J., Delucchi, K., & Hall, S. M. (2004). A meta-analysis of smoking cessation interventions with individuals in substance abuse treatment or recovery. Journal of Consulting and Clinical Psychology, 72, 1144–1156.

Prochaska, J., & DiClemente, C. C. (1983). Stages and processes of self-change of smoking: Toward an integrative model of change. Journal of Consulting and Clinical Psychology, 51, 390–395.

United States Department of Health Human Services. (2008). Evidence. In Treating tobacco use and dependence. Clinical practice guidelines.



The notion that smoking tobacco is injurious to the body is not recent. King James I of England, in his classic Counterblaste to Tobacco, written in 1604, outlined a number of beliefs about tobacco's ill effects on health and urged his subjects to avoid it. He called smoking a “filthie noveltie … A cus-tome lothsome to the eye, hatefull to the nose, harmefull to the braine, dangerous to the Lungs.” Opinions on the possible benefits and health damage caused by use of tobacco varied over the next three hundred years. Some nineteenth-century arguments that tobacco use injured health were linked to moral arguments against its use rather than to medical evidence (Corti, 1932).

In 1926, Sir Humphrey Rolleston of Cambridge University, who headed a committee on the use of Page 119  |  Top of Articleopioids, addressed the Harrogate Medical Society on the subject of medical aspects of tobacco and the possible toxic effects of nicotine (Rolleston, 1926). He drew few conclusions. Only a few health problems were clearly linked to tobacco: irritation of the throat and upper air passages by furfural, pyridine derivatives, ammonia, and carbon monoxide, which he ascribed to combustion of vegetable material and “not, like nicotine, in any way special to tobacco.” Among the heart disorders Rolleston mentioned were extrasystoles (irregular heartbeats) and angina (pain caused by insufficient blood reaching the heart muscle). He noted that nicotine constricted the coronary arteries but suggested that people who suffered from extrasystoles might consider giving up coffee and tea before tobacco. He observed that cigarette smoking could cause arterial spasms and it was linked to obliterative diseases of the large arteries among young Jews living in London's East End. Rolleston believed that cancers of the lip and oral cavity observed in smokers were probably caused by syphilis and therefore not firmly linked to smoking. He devoted only a few lines to smoking's adverse effects on the respiratory tract, observing that smoking was responsible for “causing cough, hoarseness, bronchial catarrh, and so emphysema of the lungs.” In general, Rolleston observed that considering “the large number of heavy smokers, the comparative rarity of undoubted lesions due to smoking is remarkable.” He concluded that “to regard tobacco as a drug of addiction may be all very well in a humorous sense, but it is hardly accurate.”

By the late nineteenth century, tobacco use was widespread, but people used very small amounts, mostly in the form of pipes, hand-rolled cigars, chew, and snuff; smoking was rare. The low level (by twenty-first century standards) of cigarette consumption changed dramatically at the beginning of the twentieth century with the invention of the cigarette rolling machine and the safety match. In addition to these technological innovations, the aggressive marketing campaign beginning in the late 1880s led to a dramatic increase in cigarette consumption. Before 1925, marketing was targeted exclusively at men; afterward, marketing was also targeted at women.

The turning point in the public's perception of the adverse consequences of tobacco smoking came with the publication of the Report of the Royal College of Physicians in England in 1962 and the Report of the Surgeon General in the United States in 1964. These two reports documented the experimental, epidemiological, and pathological evidence linking tobacco smoking to a variety of diseases, the most notable of which were chronic obstructive pulmonary disease (COPD), lung cancer, and illness and death from heart disease. Many more reports on the health consequences of smoking followed these two pivotal publications. Since 1969, the Office of Smoking and Health of the U.S. Public Health Service has coordinated the annual publication of a Surgeon General's Report on the health consequences of smoking, with several of the reports focusing on specific topics. In approaching such major reviews of specific health consequences of smoking, the Office of Smoking and Health assigns recognized experts to review and summarize all the existing scientific literature on the topic and then draw some conclusions from it. Some of the special topics that have been considered are the changing cigarette (the implications for health of low tar/nicotine cigarettes and filters) (1981), chronic obstructive lung disease (1984), cancer and chronic lung disease in the workplace (1985), nicotine addiction (1988), tobacco use among young people (1994), women and smoking (2001), and the health consequences of involuntary exposure to tobacco smoke (2006).

The 1979 and 1989 reports were overall reviews of the field, marking the fifteenth and twenty-fifth anniversaries of the landmark 1964 report produced when Dr. Luther Terry was Surgeon General. The 1979 report described tobacco smoking as “the largest preventable cause of death in America.” In a 2004 report, tobacco smoking was expected to cause 170,000 cancer deaths; up to 200,000 deaths from cardiovascular disease; and more than 101,000 deaths from chronic pulmonary disease in 2008 (U.S. Department of Health and Human Services, 2004). As of 2008, cigarette smoking remained the most important cause of preventable disease and premature death in developed countries. It is estimated that, depending on the age at which a person starts to smoke, seven to thirteen years of life are lost to smoking-related diseases. Nonetheless, nearly forty-five million Americans continue to smoke and the economic costs of smoking are estimated at $167 billion annually (Centers for Disease Control and Prevention, 2007).

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Other agencies, national (U.S. Environmental Protection Agency [EPA] and California Environmental Protection Agency [CalEPA]) and international (International Agency on Cancer Research [IARC]), have published comprehensive reports on tobacco and health. In particular, the CalEPA analyses tend to lead conclusions by the Surgeon General. For example, the CalEPA identified secondhand smoke (SHS) as a cause of heart disease in 1997; the Surgeon General did not do so until 2006. In 2005, the CalEPA concluded that SHS caused breast cancer in younger, primarily premen-opausal women; in 2006 the Surgeon General concluded that the evidence is suggestive (one step below causal) (California Environmental Protection Agency, 2005, p. ES-4).


Nicotine, the addictive component in tobacco, is responsible for the effects of tobacco use on the neural, cardiovascular, endocrine, and skeletal muscle systems. The most important effects are on the brain. It has stimulant (increased attentiveness, heart rate, and blood pressure) and mild depressant effects. Its effects are determined by the dose and rate of administration, hosts' tolerance, and rate of elimination. The addictive nature of nicotine is demonstrated by the return to smoking by those who have had serious smoking-related illnesses. Further, among those who quit, fewer than 10 percent are abstinent one year later (Benowitz, 2008). Pure nicotine is a poison that can kill within minutes by causing respiratory failure. Nicotine poisoning most commonly results from accidental ingestion of insecticides containing nicotine. A fatal dose of nicotine for an adult is forty to sixty milligrams.

Nicotine is quickly absorbed through the skin, mucous membranes, and lungs. Absorption through the lungs produces measurable effects on the central nervous system in as little as seven seconds. This rapid rate of absorption means that each puff on a cigarette produces some reinforcement of the smoking habit.

As early as 1963, scientists within Brown & Williamson and BAT Industries (formerly British American Tobacco) recognized that nicotine was addictive (Slade et al., 1995). In response to the public concerns about the health dangers of smoking, the tobacco industry has developed and marketed low tar and low nicotine cigarettes. Given nicotine's addictive nature, people smoke to maintain a target level of nicotine in their blood, and respond to low nicotine cigarettes by increasing their amount smoked or the number of puffs per cigarette, or by puffing more deeply or inhaling longer. Therefore, any possible benefits from switching to lower tar or nicotine cigarettes may be offset by this tendency of smokers to adjust their smoking behavior to maintain blood nicotine levels.


Cancer. Tobacco smoking has been shown to be the major cause of lung cancer in both men and women. The increased risk for lung cancer depends on the number of cigarettes smoked per day, the degree of inhalation, and the age at which the adult began smoking. The risk of death from lung cancer is about twenty times greater for men who smoke two packs a day than for those who have never smoked. It is about ten times higher for those who smoke one-half to one pack a day. Mentholated and low tar cigarettes have also been shown to increase the risk of lung cancer. Tobacco smoking is synergistic (produces a multiplier effect) with the effects of other carcinogenic risks, such as exposure to radon or asbestos. Smoking is also synergistic with alcohol in causing cancers of the oral cavity, larynx, pharynx, and esophagus. In addition, smoking has been found to increase the risk of breast cancer, particularly in young premenopausal women and those who start smoking in their teen years when the breast is still developing.

Cardiovascular Disease. Smoking is the major cause of coronary heart disease (CHD); risk of death from CHD is 70 percent higher for men who smoke, with a similar effect for women. The risk of CHD from smoking is mediated through increases in blood pressure, oxygen demand, heart rate, and oxidative stress. In addition, it decreases the blood's oxygen carrying capacity and the ability of muscle to convert oxygen into energy. Smoking increases the risk for stroke. For example, women who smoke twenty-five cigarettes or more per day have a risk for stroke almost four times higher than nonsmokers. Smoking also increases the risk of atherosclerosis (formation of plaques) in the Page 121  |  Top of Articleperipheral arteries and the aorta. In addition, it leads to arterial endothelial dysfunction. The endo-thelium, which is the arterial layer that comes into direct contact with blood, is vital for arterial dilation and contraction, and prevents cholesterol from sticking to the arterial wall.

Lung Disease. Chronic obstructive pulmonary disease (COPD) includes three related disorders: chronic mucous hypersecretion that causes cough and phlegm production; airway thickening and obstruction of expiratory airflow; and emphysema—abnormal dilation of alveoli (air sacs responsible for gas exchange) and destruction of their walls. Cigarette smoking is the major cause of COPD. Compared to nonsmokers, male smokers are three times more likely and female smokers are twice as likely to have a persistent cough.

Other Medical Disorders. Other medical disorders include peptic ulcers, upper respiratory infections, osteoporosis, erectile dysfunction, dental and eye diseases, and cancers of the pancreas, bladder, and esophagus.

Conclusions Regarding Causality. Over time, the strength of the evidence linking tobacco with disease has mounted, new conclusions have been added, and older conclusions strengthened. To summarize conclusions regarding causality, both the Surgeon General and the CalEPA have followed the classification used by the Institute of Medicine and IARC. In this classification, a four-level hierarchy is established based on the available evidence (U.S. Department of Health and Human Services, 2004, pp. 17–29).

Category A. Evidence is sufficient to infer a causal relationship: Cancers of the lung, larynx, pharynx (oral cavity), esophagus, pancreas, bladder and kidney, cervix, stomach, and acute myeloid leukemia. Coronary heart disease (including heart attacks), stroke, and aortic aneurysms are also under this category. In addition, acute respiratory illnesses (including pneumonia) and chronic obstructive pulmonary disease are included. Breast cancer, as evidenced by research published after the year 2000, has also been found to be increased by smoking (Johnson, 2005).

Category B. Evidence is suggestive of a causal relationship: Cancers of the colon and liver, and erectile dysfunction.

Category C. Evidence is inadequate to infer the presence or absence of a causal relationship: Ovarian cancer, asthma onset in adulthood, and congenital malformations in general.

Category D. Evidence is suggestive of no causal relationship: Prostate cancer.

The effects of tobacco use are not limited to specific diseases that lead to death. Tobacco use can stimulate enzymes in the liver, which can result in alterations in the way various medications are metabolized. This alteration in metabolism can mean that the levels of medications in the body will not be high enough to be optimally therapeutic.

The risk for most diseases can be decreased by smoking cessation, but not all risks decline at the same rate. Cardiovascular disease risk falls halfway back to that of a never-smoker in just one year, and is almost (but not entirely) gone within three to five years. The risk of cancer declines more slowly, with some elevated risk still evident ten years after cessation. Within five years of quitting, overall risk of premature death drops by 50 percent (Shopland & Burns, 1993).

Pipe and cigar smokers are also at an increased risk of premature death, with approximately the same relative risk as cigarette smokers of getting laryngeal and esophageal cancers. The mortality risk for users of smokeless tobacco (oral snuff and chewing tobacco) comes primarily from cancers of the oral cavity and throat (U.S. Department of Health and Human Services, 2004).

Psychiatric Disorders. Dependence on tobacco is associated with dysthymic disorder and other forms of depression. As of 2008, it is not known, however, whether depression prompts people to begin smoking or whether it develops in the course of dependence on tobacco. Mood disorders increase significantly during withdrawal from nicotine, and are common reasons for relapse.


Women who smoke tobacco have the same risks for adverse effects as men. In 2007, deaths due to lung cancer among women exceeded deaths from breast cancer, becoming the leading cause of cancer death Page 122  |  Top of Articlefor women. Some women are at special risk. Women who smoke and use oral contraceptives have an increased risk of cardiovascular disease, as well as cerebrovascular disease, including subarach-noid hemorrhage (bleeding between the brain and its protective covering inside the skull). In addition, women who start smoking early in their teen years also have an increased risk of breast cancer compared to nonsmoking women (California Environmental Protection Agency, 2005, p. ES-4).

Women who smoke have higher infertility rates than those who do not and are also more likely to have menstrual irregularities. They also have higher rates of ectopic pregnancy (abnormal implantation of the fertilized ovum outside of the uterus). Nicotine crosses the placenta, and because it constricts blood vessels, a decreased amount of oxygen is delivered to the fetus. In addition, smoking elevates the amount of carbon monoxide in the mother's blood so that it carries less oxygen to the fetus. Women who smoke during pregnancy have higher rates of premature detachment of the placenta (abruptio placentae), premature rupture of membranes, and preterm delivery. The greater the amount of tobacco smoked during the pregnancy, the higher the frequency of spontaneous abortion and fetal death and the greater the likelihood of delivering an infant that is smaller than normal. In the United States, smoking has been associated with a 20 percent increase in preterm births among women who smoked a pack a day or more compared with those who did not smoke. Women who stop smoking early in pregnancy increase their likelihood of having normal deliveries and normal birth weight babies (U.S. Department of Health and Human Services, 2001).


Secondhand smoke, also known as environmental tobacco smoke, is the smoke breathed by nonsmokers and is a mixture of mainstream (inhaled by the smoker) and sidestream (emitted from the tip of the cigarette) smoke. SHS accounts for approximately fifty thousand deaths annually, including three thousand deaths from lung cancer and forty-six thousand deaths from heart disease (U.S. Department of Health and Human Services, 2006). It has been established as a cause of heart disease, lung and sinus cancer, respiratory problems in children (bronchitis and pneumonia, middle ear infections) and adults (asthma induction), and low birth weight and sudden infant death syndrome in newborns. Passive smoke exposure during pregnancy (e.g., living with a smoker) can adversely affect the birth weight of the baby. In addition, SHS is a cause of breast cancer in young, primarily premeno-pausal, women (California Environmental Protection Agency, 2005, p. ES-4). The cardiovascular system is particularly sensitive to the harmful effects of SHS (just thirty minutes of exposure is enough to harm the exposed individual's arteries) (Barnoya & Glantz, 2005).

Exposure to SHS during pregnancy is associated with a decrease in birth weight of twenty to one hundred grams. Infants born to mothers who smoke are far more likely to die before their first birthday, primarily as a result of respiratory complications and sudden infant death syndrome. Children of mothers who smoke seem in general more likely to suffer from colds, asthma, bronchitis, pneumonia, and other respiratory problems (California Environmental Protection Agency, 2005).

Tobacco control programs (tax increases, banning smoking in the workplace and advertising, smoking cessation programs, and other strategies) have led to a reduction in the prevalence of smoking in the United States. Banning smoking in the workplace has proven to be one of the most effective tobacco control strategies, as it decreases smoking prevalence, the number of cigarettes smoked by continuing smokers, and exposure to SHS (Fichtenberg, 2002). In addition, heart disease and lung cancer mortality decrease after the implementation of smoke-free environments (Fich-tenberg, 2002; Barnoya & Glantz, 2004). To halt the spread of smoke-free legislation in the United States and worldwide, the tobacco industry has implemented several strategies, including hiring scientists to redirect public attention from SHS toward other sources of air pollution, lobbying politicians, and creating useless smoking and nonsmoking sections in public places.

In general, white males in higher socioeconomic groups have lowered their smoking rate more than women and members of ethnic and racial minorities and lower socioeconomic groups. Adult smoking prevalence in the United States Page 123  |  Top of Articleremained unchanged during the early 1990s but decreased from 1997 (24.7%) to 2004 (20.8%). Smoking prevalence by ethnic group is highest among American Indians/Alaska Natives (32%), followed by African Americans (23%), Whites (22%), Hispanics (15%), and Asians (10%) (Centers for Disease Control and Prevention, 2007). An estimated 20 percent of high school students (ninth to twelfth grades) were current smokers in 2005 (Centers for Disease Control and Prevention, 2006).

In contrast to the general decline in the prevalence of smoking in developed nations, the prevalence of smoking is increasing in developing and newly industrialized countries. By the year 2030, cigarettes will kill ten million people per year; 70 percent of this total will be in low- and middle-income countries (Jha & Chaloupka, 1999). In most of these countries, the tobacco industry has been successful in preventing the implementation of sound tobacco control measures.

See also Advertising and Tobacco Use; Complications; Nicotine; Treatment, Behavioral Approaches to; Treatment, Pharmacological Approaches to; Treatment, Specialty Approaches to.


Barnoya, J., & Glantz, S. A. (2004). Association of the California tobacco control program with declines in lung cancer incidence. Cancer Causes Control, 15, 689–695.

Barnoya, J., & Glantz, S. A. (2005). Cardiovascular effects of secondhand smoke: nearly as large as smoking. Circulation, 111, 2684–2698.

Benowitz, N. L. (2008). Neurobiology of nicotine addiction: Implications for smoking cessation treatment. The American Journal of Medicine Update on Smoking Cessation Interventions for the Primary Care Physician, 121, S3–S10.

California Environmental Protection Agency. (2005). Proposed identification of environmental tobacco smoke as a toxic air contaminant. State of California: Office of Environmental Health Hazard Assessment.

Centers for Disease Control and Prevention. (2007). Cigarette smoking among adults: United States, 2006, 53, 1157–1161. Atlanta, GA: Author.

Centers for Disease Control and Prevention. (2006). Cigarette use among high school students: United States 19912005, 55, 724–726. Atlanta, GA: Author.

Corti, E. (1932). A history of smoking (P. England, Trans.). New York: Harcourt, Brace.

Fichtenberg, C. M., & Glantz, S. A. (2002). Association of the California Tobacco Control Program with declines in cigarette consumption and mortality from heart disease. New England Journal of Medicine, 343, 1772–1777.

Fichtenberg, C. M., & Glantz, S. A. (2002). Effect of smoke-free workplaces on smoking behaviour: Systematic review. British Medical Journal, 325, 188–191.

Jha, P., & Chaloupka, F. J. (1999). Curbing the epidemic. Governments and the economics of tobacco control. Washington, DC: The World Bank.

Johnson, K. C. (2005). Accumulating evidence on passive and active smoking and breast cancer risk. International Journal of Cancer, 117, 619–628.

Rolleston, H. (1926, May 22). Medical aspects of tobacco. Lancet, 1, 961–965.

Shopland, D. R., & Burns, D. M. (1993). Medical and public health implications of tobacco addiction. In C. T. Orleans & J. Slade (Eds.), Nicotine addiction: Principles and management. New York: Oxford University Press.

Slade, J., Bero, L. A., Hanauer, P., Barnes, D. E., & Glantz, S. A. (1995). Nicotine and addiction. The Brown and Williamson documents. Journal of the American Medical Association, 274, 225–233.

U.S. Department of Health and Human Services. (2001). Women and smoking: a report of the Surgeon General. Washington, DC: Office of the Surgeon General.

U.S. Department of Health and Human Services. (2004). The health consequences of smoking. A report of the Surgeon General. Washington, DC: Centers for Disease Control and Prevention; National Center for Chronic Disease Prevention and Health Promotion; Office on Smoking and Health.

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.



Tobacco has been used in various nonsmoked forms throughout its long history. Indeed, before the introduction of the mass-produced cigarette in the early twentieth century, smokeless tobacco, Page 124  |  Top of Articleincluding chewing tobacco and snuff, was the predominant form of tobacco use, and in some regions of the world, such as India, it remains so in the early twenty-first century.

The earliest uses of tobacco, dating back thousands of years, were probably through chewing the leaves of the plant or inhaling powdered tobacco through the nose (snuffing). Tobacco was held to have many uses among Native Americans, including as a medicine, wound healer, appetite suppressant, psychoactive agent, and as an aid to religious rituals.

Early Spanish explorers recorded their observations of the practice of chewing and snuffing tobacco among the natives as well as smoking. When tobacco was brought back to Europe it was used both in smoked form (cigars and pipes) and in smokeless forms. However, during the eighteenth and early nineteenth centuries, tobacco use in European society was most commonly in the form of snuff. The practice of snuffing became fashionable among the French aristocracy at the time. The offering and taking of snuff in social settings became highly stylized, and elaborate snuff boxes served to display one's refinement, rank and wealth. Snuff use subsequently gained broader popularity in other European countries, including England, and outside the elite circles.

In late nineteenth century America, chewing tobacco was widespread and at its peak of popularity. Spittoons became a fixture in many public places, such as public buildings and trains. In the early twentieth century, however, use of chewing tobacco declined as machine-rolled cigarettes, which were seen as more convenient and hygienic, gained popularity. Around 1900, 52 percent of all tobacco used in the United States was smokeless, but by 1952 that number had dropped to 6 percent (Lewis et al., 1999).


The term smokeless tobacco refers to an extremely diverse range of products, including mass-produced manufactured products as well as traditional and handmade products. While smokeless tobacco products by definition contain tobacco as the principal ingredient, the tobacco may also be mixed with other ingredients. For example, the primary ingredients in gutka, which is widely used in the Indian subcontinent, include betel leaf, areca nut, and a variety of spices and flavors in addition to tobacco. Even within the United States, a wide range of different types of smokeless tobacco products with different characteristics are used, including chewing tobacco, dry and moist snuff, traditional oral tobacco products, such as iqmik, and novel products, such as tobacco lozenges. The popularity of different product types has evolved over time. For example, use of moist snuff or dip increased substantially toward the end of the twentieth century, making up over half of the smokeless tobacco market, whereas sales of chewing tobacco and dry snuff fell (Maxwell, 2004).

Overall sales in pounds of smokeless tobacco products in the United States have remained relatively unchanged, or saw only a slight decline, between 1988 and 2008. However, revenues and advertising and promotional expenditures increased steadily over the same period. In 2005, the five largest tobacco manufacturers spent $250.76 million on smokeless tobacco advertising and promotion; over 40 percent of that was spent on price discounts paid to retailers and wholesalers to reduce the price to consumers for smokeless tobacco products (Federal Trade Commission, 2007, pp. 3, 5).

According to the 2006 National Survey on Drug Use and Health, there are approximately 8.2 million people aged 12 or older in the United States who use smokeless tobacco. The prevalence of smokeless tobacco use in the U.S. population overall is substantially lower (3.3%) than that for cigarette smoking (25%). However, there are substantial disparities in smokeless tobacco use among subgroups of the population. While 6.6 percent of American males report current smokeless use, only 0.3 percent of American females report the same. Smokeless tobacco use is also substantially higher among whites (4.2%) and American Indian/Alaska Natives (6.5%) than among African Americans (1.7%), Asians (1.2%), and Hispanics (0.9%). Smokeless tobacco use is greater in rural areas; the proportion of smokeless tobacco use ranges from 10 percent in rural counties to only 2 percent in large metropolitan counties (Substance Abuse and Mental Health Services Administration, 2007). High prevalence of smokeless tobacco use has also been found among U.S. military personnel (24% reported use; Chisick et al., 1998) and among some athletes, particularly major league baseball players (36% reported use; Severson et al., 2005).

Page 125  |  Top of Article

Use of smokeless tobacco among youth warrants particular attention both because its prevalence is higher and because it may serve as a pathway to nicotine addiction and use of other tobacco products. A national survey found that 12.6 percent of twelfth grade boys reported having used smokeless tobacco in the past 30 days, and prevalence was even higher among white boys in southern states (Nelson et al., 2006, p. 900). Moreover, some smokeless tobacco products may be more accessible to new users and more likely to appeal to adolescents. During the 1970s, smokeless tobacco use increased substantially among teens and young adults when new products were introduced that were more accessible to new users, with lower nicotine content and attractive flavorings (Connolly, 1995). And evidence suggests that users who begin with starter products, that are low in nicotine, are more likely to graduate subsequently to products with higher nicotine content (Tomar et al., 1995).

A number of studies suggest that adolescents who use smokeless tobacco may be more likely to progress to cigarette smoking, although the evidence is not consistent (Tomar, 2003; O'Connor et al., 2005; Haddock et al., 2001). Smokeless tobacco also poses a global public health challenge. In many regions of the world, such as in India, smokeless tobacco use is the predominant form of tobacco use. In the Indian National Family Health Survey, 20 percent (28.1% of men and 12.0% of women) of respondents reported chewing tobacco and/or pan masala, though these figures varied widely by region (Rani et al., 2003, p. 3). Also, data from the Global Youth Tobacco Survey show that students aged 13 to 15 surveyed in 132 countries were more likely to report using non-cigarette tobacco products (11.2%) than to report smoking cigarettes (8.9%; MMWR, 2006).


One International Agency for Research on Cancer (IARC) monograph on smokeless tobacco reported that there is sufficient evidence, based on epidemiologic and laboratory studies, to conclude that smokeless tobacco causes oral cancer and pancreatic cancer in humans (Cogliano et al., 2004). At least 28 different carcinogens have been identified in smokeless tobacco products (National Cancer Institute, 1992, p. 115). Additionally, measurements of carcinogen by-products in humans show that smokeless tobacco users are exposed to levels of tobacco-specific nitros-amines, among the most important tobacco carcinogens, that are as high or higher than cigarette smokers (Kresty et al., 1996). There is also limited but inconsistent evidence suggesting that smokeless tobacco use may be associated with cardiovascular disease (Gupta et al., 2004). And smokeless tobacco use is associated with other health outcomes, including oral mucosal lesions, leukoplakia, and periodontal disease.

However, assessing the health risks of smokeless tobacco products is complicated given the diversity of traditional and manufactured products in use and their different characteristics. One study of eleven smokeless tobacco product brands available in the United Kingdom found that levels of tobacco-specific nitrosamines varied 130-fold across the products and nicotine content ranged from 0.1 mg/g to 63.2 mg/g (McNeill et al., 2006). Additionally, moist snuff sold in Sweden has relatively low levels of nitrosamines compared with some other smokeless tobacco products, such as American chewing tobacco (Hoffman et al., 1995) or toombak, a moist snuff product found in Sudan (Idris et al., 1991). Moreover, the health risks experienced by any tobacco user vary depending not only on the type of product used but on how it is used, when the person started and/or quit, and concurrent use of other harmful substances.


Smokeless tobacco products contain nicotine as a major constituent and users of smokeless tobacco products demonstrate signs of dependence similar to those in cigarette smokers, including tolerance with repeated use and symptoms of withdrawal upon cessation of use. Moreover, individuals who are dual users (those who use both cigarettes and smokeless tobacco) tend to have higher nicotine exposure levels and find cessation even more difficult to achieve than those who use only one type of product (Wetter et al., 2002).

However, the most promising strategies for helping smokeless tobacco users to quit are different than those for cigarette smoking. While drug interventions, including nicotine replacement therapy (such as nicotine patch or gum) and bupropion, have been shown to be effective in helping cigarette smokers to quit, studies in smokeless Page 126  |  Top of Articletobacco users have not found a similar benefit (Ebbert et al., 2004). These treatments may help reduce unwanted side effects associated with nicotine withdrawal, such as feelings of craving or weight gain, but they have not been shown to have any impact on successful quitting over the long term (Dale et al., 2007). Yet there is strong evidence that behavioral counseling interventions are effective for helping smokeless tobacco users to quit. In particular, counseling patients in dental offices, where the effects of smokeless tobacco use on the mouth can be detected and explained, has been shown to increase success in quitting. Interestingly, similar interventions have not been found to be effective for cigarette smokers (Carr & Ebbert, 2006). Telephone counseling may also be useful in assisting smokeless tobacco users to quit, although larger studies are needed to support more specific recommendations. In general, the evidence regarding cessation in smokeless tobacco users is very limited compared to that for cigarette smoking.


While smokeless tobacco use causes cancer and other diseases, it is associated with a lower overall risk profile compared with cigarette smoking. Indeed, according to some estimates, the magnitude of this difference is vast (i.e., “consumption of non-combustible tobacco is of the order of 10-1,000 times less hazardous than smoking” according to Royal College of Physicians, 2002, p. 5). This difference has led some scientists to suggest that smokeless tobacco has promise as a harm reduction intervention for cigarette smokers. That is, smokers who have trouble quitting might reduce their risk by switching to a smokeless tobacco product in place of cigarettes. However, there is not sufficient evidence as of 2008 to demonstrate that this strategy is effective in practice. In other words, even if the product is less toxic, it is not clear whether smokers will successfully switch without relapsing or continuing to smoke. Critics of this approach have also suggested that promoting the use of smokeless tobacco as less harmful might lead to an increase in initiation of smokeless tobacco use by adolescents and other new users or have a negative impact on tobacco use cessation efforts (Hatsukami et al., 2004).

The Swedish Experience is often referred to as a sort of natural experiment in the use of smokeless tobacco for harm reduction (Foulds et al., 2003). Sweden has the lowest male smoking prevalence of any country in Europe (14% of adult men are daily smokers) and the lowest levels of tobacco related mortality (about half that of the EU overall). However, a significant portion of men (22%) report using oral smokeless tobacco, typically in the form of snus, a moist oral tobacco product. Some scientists have suggested that the low smoking prevalence (and lower mortality) is due to the use of snus in place of cigarettes. However, this trend may also be a result of broader social and policy influences. For example, in the early 1960s Sweden was one of the first countries to fund an organized tobacco control effort, including the development of cessation clinics and antismoking education programs (Mitchell & Wellings, 1998). Changes in popular culture also likely had an impact on behavior and national smoking trends, as popular portrayals of smoking shifted from accepting to negative (Torell, 2002).


In the late 1990s and early twenty-first century, a range of new smokeless tobacco products were introduced and marketed that may be more likely to appeal to new users, including youth. Some new smokeless products use attractive flavorings, such as mint or fruit flavors, and new delivery methods, such as lozenges or small pouches that eliminate the need to spit. Major cigarette manufacturers Philip Morris and R. J. Reynolds have also introduced new smokeless tobacco products using the familiar brand names Marlboro and Camel. Moreover, some smokeless tobacco manufacturers have introduced new marketing strategies, such as marketing smokeless tobacco products to smokers for situations in which they cannot smoke, given the increase in smoking restrictions in workplaces and public spaces (O'Hegarty et al., 2007). It remains to be seen as of 2008 whether these new strategies will lead to increased use of smokeless tobacco.

Policies and regulations around smokeless tobacco products vary widely across countries. Additionally, the policies and regulations applying to smokeless tobacco products are in many cases different than those for cigarettes. For example, in the United States smokeless tobacco product packages carry a different set of mandated health warnings than cigarette packages. Additionally, smokeless tobacco Page 127  |  Top of Articleproducts are taxed differently than cigarettes; in general they are taxed at a lower level and states use different formulas for calculating the taxes. Since 2001, the European Union has prohibited marketing of snuff products (but not cigarettes or chewing tobacco) in all affected countries except Sweden and Norway. However, the World Health Organization Framework Convention on Tobacco Control, the first global public health treaty, broadly applies to all tobacco products, including traditional and manufactured forms of smokeless tobacco.

See also Advertising and Tobacco Use; Withdrawal: Nicotine (Tobacco).


Carr, A. B., & Ebbert, J. O. (2006). Interventions for tobacco cessation in the dental setting. Cochrane Database of Systematic Reviews, Issue 1. Art. No.: CD005084. DOI: 10.1002/14651858.CD005084.pub2.

Chisick, M. C., Poindexter, F. R., & York, A. K. (1998). Comparing tobacco use among incoming recruits and military personnel on active duty in the United States. Tobacco Control, 7, 236–240.

Cogliano, V., Straif, K., Baan, R., Grosse, Y., Secretan, B., & El Ghissassi, F. (2004). Smokeless tobacco and tobacco-related nitrosamines. Lancet Oncology Journal, 5, 708.

Connolly, G. (1995). The marketing of nicotine addiction by one oral snuff manufacturer. Tobacco Control, 4, 73–79.

Dale, L. C., Ebbert, J. O., Glover, E. D., Croghan, I. T., Schroeder, D. R., Severson, H. H., et al. (2007). Bupropion SR for the treatment of smokeless tobacco use. Drug and Alcohol Dependence, 90, 56–63.

Ebbert, J. O., Rowland, L. C., Montori, V., Vickers, K. S., Erwin, P. C., Dale, L. C., et al. (2004). Interventions for smokeless tobacco use cessation. Cochrane Database of Systematic Reviews, Issue 3. Art. No.: CD004306. DOI: 10.1002/14651858.CD004306.pub2.

Federal Trade Commission. (2007). Smokeless tobacco report for the years 2002–2005. Washington, DC: Author. Available from

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.

Gupta, R., Gurm, H., & Bartholomew, J. R. (2004). Smokeless tobacco and cardiovascular risk. Archives of Internal Medicine, 164, 1845–1849.

Haddock, C., Weg, M., DeBon, M., Klesges, R., Talcott, G., Lando, H., et al., (2001). Evidence that smokeless tobacco use is a gateway for smoking initiation in young adult males. Preventive Medicine, 32, 262–267.

Hatsukami, D. K., Lemmonds, C., & Tomar, S. L. (2004). Smokeless tobacco use: Harm reduction or induction approach? Preventive Medicine, 38(3), 309–317.

Hoffmann, D., Djordjevic, M. V., Fan, J., Zang, E., Glynn, T., & Connolly, G. N. (1995). Five leading U.S.commercial brands of moist snuff in 1994: Assessment of carcinogenic N-nitrosamines. Journal of the National Cancer Institute, 87, 1862–1869.

Idris, A. M., Nair, J., Oshima, H., Friesen, M., Brouet, I., Faustman, E. M., et al., (1991). Unusually high levels of carcinogenic nitrosamines in Sudan snuff (Toom-bak). Carcinogenesis, 12, 1115–1118.

Kresty, L. A., Carmella, S. G., Borukhova, A., Akerkar, S. A., Gopalakrishnan, R., Harris, R. E., et al. (1996). Metabolites of a tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), in the urine of smokeless tobacco users: Relationship between urinary biomarkers and oral leukoplakia. Cancer Epidemiology Biomarkers and Prevention, 5(7), 521–525.

Lewis, P. C., Harrell, J. S., Deng, S., & Bradley, C. (1999). Smokeless tobacco use in adolescents: The cardiovascular health in children (CHIC II) study. Journal of School Health, 69, 320–335.

Maxwell, J. C., Jr. (2004). The Maxwell report: The smokeless tobacco industry in 2003. Richmond, VA: John C. Maxwell Jr.

McNeill, A., Bedi, R., Islam, S., Alkhatib, M. N., & West, R. (2006). Levels of toxins in oral tobacco products in the UK. Tobacco Control, 15(1), 64–67.

Mitchell, K., & Wellings, K. (1998). Improving health status in Europe: A case study approach to the identification of best practice. Best practice in smoking: The Swedish Case Study. London School of Hygiene and Tropical Medicine.

Morbidity and Mortality Weekly Report. (2006). Use of cigarettes and other tobacco products among students aged 13–15 years worldwide, 1999–2005. Morbidity and Mortality Weekly Report, 55, 553–556.

National Cancer Institute. (1992). Monograph 2: Smokeless tobacco or health: An international perspective. Bethesda, MD: U.S. Department of Health and Human Services, National Cancer Institute. Available from .

Nelson, D. E., Mowery, P., Tomar, S., Marcus, S., Giovino, G., & Zhao, L. (2006). Trends in smokeless tobacco use among adults and adolescents in the United States. American Journal of Public Health, 96, 897–905.

O'Connor, R. J., Kozlowski, L. T., Quinio Edwards, B., & Flaherty, B. P. (2005). Most smokeless tobacco use does not cause cigarette smoking: Results from the Page 128  |  Top of Article2000 National Household Survey on Drug Abuse. Addictive Behaviors, 30, 325–336.

O'Hegarty, M., Richter, P., & Pederson, L. L. (2007). What do adult smokers think about ads and promotional materials for PREPs? American Journal of Health Behaviors, 31, 526–534.

Rani, M., Bonu, S., Jha, P., Nguyen, S. N., & Jamjoum, L. (2003). Tobacco use in India: Prevalence and predictors of smoking and chewing in a national cross sectional household survey. Tobacco Control, 12(4), e4.

Royal College of Physicians, Tobacco Advisory Group. (2002). Protecting smokers, saving lives: The case for a tobacco and nicotine regulatory authority. London: Royal College of Physicians.

Severson, H. H., Klein, K., Lichtensein, E., Kaufman, N., & Orleans, C. T. (2005). Smokeless tobacco use among professional baseball players: Survey results, 1998 to 2003. Tobacco Control, 14, 31–36.

Substance Abuse and Mental Health Services Administration. (2007). Results from the 2006 National Survey on Drug Use and Health: Detailed tables. Available from .

Tomar, S. (2003). Is use of smokeless tobacco a risk factor for cigarette smoking? The U.S. experience. Nicotine & Tobacco Research, 5(4), 561–569.

Tomar, S. L., Giovino, G. A., & Eriksen, M. P. (1995). Smokeless tobacco brand preference and brand switching among U.S. adolescents and young adults. Tobacco Control, 4, 67–72.

Torell, U. (2002). Den rökande människan: bilden av tobaksbruk i Sverige mellan 1950- och 1990-tal. Stockholm: Carlsson bokförlag.

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Successful smoking cessation is associated with modest weight gain. The amount of weight gain tends to average 10 to 13 pounds in the first year after quitting, with most of this occurring within the first six months of abstinence. Individual characteristics influencing the amount of weight gain include gender and initial body weight, length and frequency of smoking behaviors, and other lifestyle factors such as type of diet and physical activity. The exact mechanism through which cigarette smoking affects energy expenditure and body weight is not fully understood and is likely a combination of several factors:

There is a slight metabolic advantage to cigarette smoking, meaning that smoking increases heart rate and the overall level of energy that the body uses to function. Following cessation, basal metabolic level slows, which promotes weight gain.

Smoking suppresses appetite and food intake. Animal research has shown that mice administered nicotine initially eat less than control mice but that meal size eventually increases. Similarly, some dieters attempt to use the appetite-suppressing effects of smoking to resist urges to eat and to help them eat less. However, over the long term smokers do not tend to eat less than nonsmokers.

Following smoking cessation, food smells and tastes better and is, therefore, more desirable. In general, smoking serves as an appetite suppressant and during withdrawal from nicotine, appetite increases. Laboratory experiments have shown that during smoking withdrawal, people are likely to manage cigarette cravings with food and to report more enjoyment in the experience of eating. Among current smokers, short-term abstinence from smoking is associated with heightened cravings for cigarettes and food, as well as increased calorie and fat intake.

Through a combination of these factors, smoking suppresses body weight, and following cessation weight reverts to a higher natural set point. On the population level, smokers tend to weigh less than former-smokers, who in turn weigh less than never-smokers. It should be noted that although there are certain health benefits to lower weight, these benefits are greatly offset by the negative health impact of smoking.


For some smokers, concerns about weight may motivate the decision to begin smoking. Initiation of smoking by adolescent girls has been linked to weight concerns, and among young adults smoking is more common among those who are trying to lose weight. The cigarette industry appears to Page 129  |  Top of Articlecapitalize on the weight concerns of its target market by producing advertisements that equate smoking with being slim. There is some evidence to suggest that smokers who are especially concerned about their weight have magnified beliefs in the ability of smoking to suppress weight; that is, they believe smoking to be much more effective at controlling weight than it actually is. Consequently, smokers who are especially weight concerned are less likely to report a desire to quit.

Weight concerns are also associated with unsuccessful attempts to quit smoking. One of the commonly reported reasons for smoking relapse is weight gain. Although concerns about weight gain are more common for female smokers than male, a significant portion of male smokers also report fear of cessation-associated weight gain.


Smoking cessation treatments that include a component to address weight gain may be more successful for some individuals, especially those with heightened concerns about weight gain. Several treatment options have shown some promise, whereas others have been less successful.

Behavioral treatments for weight control may be effective for weight-concerned smokers. Examples of behavioral weight control treatments include moderate calorie-reducing diets and programs to promote physical activity. These treatments are most successful when administered as a supplement to standard smoking-cessation treatment and when promoting behavioral changes intended to result in very modest weight change. The DHHS 2000 Clinical Practice Guideline for treating tobacco use and dependence recommends that patients not attempt weight control until after they are confident that they will not resume smoking. Patients should be advised that strict dieting during a quit attempt could hinder successful cessation.

Cognitive Behavioral Therapy. Cognitive behavioral therapy (CBT) and other treatments to address body image and weight concerns aim to establish healthier body image, thus reducing the psychological distress associated with slight weight gain. CBT for cessation-related weight gain draws from treatments for eating disorders and body image disturbances and helps patients learn to modify mal-adaptive thoughts that lead to unhealthy weight control. Examples of these maladaptive thoughts include overvalued ideas of the importance of thinness, and all-or-nothing thinking (e.g., that one can be only thin or overweight, or there are good and bad foods). CBT may be particularly effective as a supplement to standard treatment for women who are weight-preoccupied.

Pharmacological Treatments. Certain medications may be especially helpful for weight-concerned smokers by helping to reduce weight gain. Bupropion is an antidepressant (selective reuptake inhibitor of dopamine and noradrenalin) that is an efficacious treatment for smoking cessation. Theorized mechanisms of its effectiveness in assisting smoking cessation include its antidepressant effects and its effectiveness in reducing nicotine cravings. Bupropion also reduces appetite for food, and may effectively curb weight gain following cessation, thereby increasing the likelihood of prolonged abstinence. Research has shown that smokers experience heightened food reward following smoking cessation and that bupropion effectively attenuates this increase. Research reviews indicate that bupropion is an effective and well-tolerated first-line treatment for smoking cessation. Naltrexone hydrochloride is an opiate antagonist and may be particularly effective for reducing post-cessation weight gain due to its regulation of appetitive behaviors. When administered in conjunction with the nicotine patch, low-dose naltrexone results in less post-cessation weight gain.

Smoking cessation is associated with modest weight gain. The exact mechanism of weight gain is not fully understood but is likely a combination of physiological and behavioral factors. There is some evidence that weight-preoccupied smokers have a more difficult time quitting due to their unwillingness to tolerate minimal weight gain. Although concerns about weight gain are more common for female smokers than male smokers, a significant portion of male smokers also report fear of cessation-associated weight gain. Treatments that address weight gain may be more successful for some individuals, especially those with heightened concerns about weight gain, and may increase interest in making a quit attempt.

Page 130  |  Top of Article

See also Advertising and Tobacco; Nicotine Delivery Systems for Smoking Cessation; Treatment, Behavioral Approaches to: Cognitive-Behavioral Therapy.


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Source Citation

Source Citation   

Gale Document Number: GALE|CX2699700444