Summary of Key Points
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Tobacco is responsible for one in five deaths, and tobacco use is the single largest preventable cause of death and disability in the United States.
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Spine-related disorders are more common in smokers, and spine surgeries are up to four times more frequent in cigarette smokers.
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Symptomatic pseudarthrosis is believed to be three to five times more common in smokers than nonsmokers.
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After surgical procedures for isthmic lumbosacral spondylolisthesis or chronic low back pain, smokers were more likely to be dissatisfied and have worse results.
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Smoking is associated with increased perioperative cardiopulmonary, wound, and infection-related complications.
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In 2010, 68.8% of adult smokers wanted to stop smoking, 52.4% had made at least one quit attempt in the last year, and 6.2% were successful.
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Counseling and pharmacologic interventions have been shown to be effective in increasing cessation rates.
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Cessation rates improve significantly following physician-initiated interventions of less than 5 minutes.
Smoking is responsible for one in five deaths, and tobacco use is the single largest preventable cause of death and disability in the United States. Smoking has been linked to numerous health conditions, including cancer, respiratory disease, cardiovascular disease, and peripheral vascular disease ; however, the delayed onset of these diseases makes it difficult for users to realize the potential consequences of tobacco use until significant damage has been done. The addictive properties of tobacco use, both chemical and psychological, make cessation difficult for even the most determined quitter. Despite numerous public health efforts, tobacco use continues to have significant adverse effects on the health of people everywhere.
Tobacco use affects the entire body and has been identified as a risk factor for six of the eight leading causes of death in the world: malignancies, heart disease, cerebrovascular disease, lower respiratory infections, chronic obstructive pulmonary disease, and tuberculosis ( Table 176-1 ). Associated with increased osteoclast and decreased osteoblast activity, smoking has been implicated as a risk factor for osteoporosis, delayed fracture healing, and fusion pseudarthrosis. In general, multiple studies have indicated that spine-related disorders are more common in smokers, and spine surgeries are up to four times more frequent in cigarette smokers. Symptomatic fusion pseudarthrosis is believed to be three to five times more common in smokers than nonsmokers.
| Adverse Effect | Signs |
|---|---|
| Cancer | Lung, trachea, bronchus, oral, esophageal, stomach, colorectal, liver, pancreatic, bladder, kidney, and cervical cancers; leukemia |
| Cardiovascular | Atherosclerosis, cerebrovascular disease, coronary artery disease, myocardial infarction, abdominal aortic aneurysm |
| Dental | Implant complications and failure |
| Dermatologic | Advanced skin aging, wrinkles |
| Endocrine | Diabetes mellitus |
| Gastrointestinal | Peptic ulcer disease |
| Immunologic | Infectious disease susceptibility, tuberculosis |
| Ophthalmologic | Cataracts |
| Orthopaedic | Decreased bone mineral density, delayed fracture healing, increased fracture risk, rheumatoid arthritis |
| Respiratory | Chronic obstructive pulmonary disease, pneumonia, impaired lung development |
| Reproductive | Maternal infertility, miscarriage, low birth weight, stillbirth, sudden infant death syndrome, congenital malformations, erectile dysfunction |
| Spinal | Back and neck pain, prolonged disability, poor surgical outcomes |
| Surgical | Surgical site infections, delayed healing |
This chapter highlights specific consequences of tobacco use on the spine, including contributions to disease development and effects on treatment outcomes. It presents the current prevalence of tobacco use in the United States and recent trends. The adverse effects of tobacco use on the entire body and the physiologic effects of nicotine are discussed. Tobacco is a complex, variable substance composed of numerous chemicals; therefore, this chapter identifies the compounds typically found in tobacco smoke and examines their adverse effects. The definitions of addiction and dependence and the roles they play in the perpetuation of tobacco use are reviewed. Perhaps most important, current strategies for smoking cessation and their outcomes are discussed.
Adverse Health Effects of Tobacco Use
Initially linked to lip, mouth, and throat cancers in the 18th and 19th centuries, tobacco use has been shown to result in significant damage throughout the body. Estimates from the late 1990s indicated adult male smokers lost an average of 13.2 years of life and females lost 14.5 years of life due to smoking. A review of patients over 60 years of age found an 83% increased mortality for current smokers and a 34% increased mortality for former smokers compared to never smokers.
Typically associated with lung cancer, smoking actually results in more deaths from cardiovascular and respiratory diseases. Lung diseases linked to smoking include cancer, bronchitis, emphysema, and a predisposition for pneumonia. Injuries to the cardiovascular system resulting from smoking include coronary artery disease, myocardial infarction, cerebral vascular attack, aneurysm, and peripheral vascular disease. Coronary artery disease is two to four times more common in smokers than nonsmokers, and smokers are twice as likely to die from heart attacks as nonsmokers. In nonsmokers, exposure to secondhand smoke has been associated with a 25% to 30% increased risk for the development of coronary artery disease. Smoking has also been associated with the development of diabetes, cataracts, and bacterial infections. Smokeless tobacco has been associated with an increased risk of oral cancers, gingival recession, and oral leukoplakia.
Spine-Specific Consequences of Tobacco Use
Although smoking has been the form of tobacco use most often studied, any type of tobacco use has been shown to affect the spine adversely in multiple ways ( Table 176-2 ). Not only are tobacco users more likely to have back and neck pain or injuries, they are less likely to have significant improvement following treatment.
| Problem | Characteristics | Mechanism | References |
|---|---|---|---|
| Back and neck pain | Increased incidence in smokers Onset at younger age Symptoms more severe Symptoms more often present Attitude regarding improvement more pessimistic Dose-dependent relationship suggested | Accelerated disc degeneration Decreased blood flow to intervertebral disc due to vasoconstriction and atherosclerosis Decreased oxygen delivery due to elevated carboxyhemoglobin levels Increased levels of free radicals and toxic chemicals Decreased reparative capability of tissues Decreased production of collagen Osteoporosis-related fractures Chronic cough | |
| Arthrodesis rates | Pseudarthrosis rates increased up to 40% in smokers Dose-dependent relationship suggested | Decreased expression of genes related to bone healing Decreased blood flow and oxygen delivery | |
| Postoperative complications | Significantly increased in smokers Dose-dependent relationship suggested Smokers are more likely to require reoperation, up to 26%, with a relative risk of 2.59 Preoperative cessation significantly lowers complication rates | Decreased oxygen delivery, by up to 70% Less effective immune response Decreased collagen synthesis Increased adjacent-segment disease | |
| Postoperative outcomes | Smokers less likely to return to work, more likely to be disabled, and less satisfied with outcomes | Multifactorial | |
| Fractures | Increased risk of fractures in both males and females Dose-dependent relationship suggested Increased incidence of vertebral, hip, proximal humerus, and distal forearm fractures Earlier, by 5 years, occurrence of incident fragility fractures | Increased incidence of osteoporosis Smoking is an independent, dose-dependent risk factor Decreased body mass and altered body composition Decreased effective estrogen levels Decreased calcium absorption Decreased levels of 25-OH vitamin D Reduced bone size and decreased amounts of cancellous and cortical bone Decreased osteocyte function Increased fall risk due to physical and neuromuscular performance of someone 5 years older |
Back Pain
An estimated 15% to 20% of adults have at least one episode of low back pain every year, and 50% to 80% experience low back pain at least once in a lifetime. Similarly, neck pain is experienced by approximately 20% of the adult population in 1 year and by 66% of the population in a lifetime. A majority of evidence on the epidemiology of neck and back pain indicates that cigarette use is associated with higher rates of pain. Although authorities have suggested the existence of a causal relationship between smoking and neck and back pain, a relative lack of prospective studies makes it difficult to confirm this theory.
Compared with nonsmokers, smokers who have back pain are often younger, report more severe symptoms, and indicate that the symptoms were present for a larger portion of the day. Smokers are also more often extremely dissatisfied by their current health, more likely to report depression, more pessimistic regarding the resolution of their pain, and less likely to show a trend toward improvement following surgery. Adolescent smokers are significantly more likely to develop back pain than nonsmokers, with evidence supporting a dose-response relationship.
Disc Degeneration
Degeneration of the intervertebral disc is believed to be pivotal in the development of lower back pain. In addition to the effects of aging, variable dynamic and biologic stresses contribute to disc degeneration. Following exposure to nicotine, catecholamine-mediated vasoconstriction results in decreased blood flow to the intervertebral discs. Elevated carboxyhemoglobin levels in smokers and the expected presence of free radicals and toxic substances could further contribute to inadequate nutrition of intervertebral disc tissues. Alterations in cell morphology, increased levels of proinflammatory cytokines, decreased glycosaminoglycan levels, and decreased production of collagen with a shift toward the production of type I collagen have been demonstrated following the exposure of intervertebral disc cells to nicotine.
Chronic cough has been linked to the development of back pain in the general population, and cigarette smokers are three times more likely to have a chronic cough than people who have never smoked or who are previous smokers. Vertebral body or end plate fractures resulting from smoking-induced decreased bone mineral density are also likely to lead to back pain.
Fusion
Smoking has been associated with decreased fracture healing rates and increased incidence of nonunion; thus, it is not surprising that smokers also tend to have similar difficulties following arthrodesis procedures. A rabbit model of intertransverse process fusion found reduced fusion rates in those receiving nicotine up to the day of surgery and a 0% fusion rate in those continuing to receive nicotine postoperatively. Nicotine exposure resulted in decreased expression of genes for vascular endothelial growth factor, basic fibroblast growth factor, types I and II collagen, and bone morphogenetic protein (BMP)-2, BMP-4, and BMP-6.
Following dorsal lumbar fusion procedures, smokers have been found to have pseudarthrosis rates increased up to 40% higher than nonsmokers. Smokers able to stop prior to surgery and remain abstinent in the postoperative period have improved rates of fusion compared with people who continue to smoke. The use of rhBMP-2 has been shown to significantly increase fusion rates in smokers. Following surgery, smokers were less likely to return to full-time work, more likely to be disabled, and less satisfied with the outcome.
An analysis of results from ventral cervical arthrodesis procedures indicates that there is an increased pseudarthrosis rate following multilevel discectomy and interbody grafting using autogenous grafts in smokers compared with nonsmokers. The clinical outcome is significantly better for nonsmokers than smokers.
Surgical Complications
Surgical site infections have been reported to be more common in smokers following spine surgery, and chronic hypoxia decreases collagen synthesis and deposition in healing wounds. Published results are mixed, but smoking has also been suggested as a risk factor for the development of deep venous thromboses following surgical procedures.
Tissue oxygenation is compromised in smokers due to multiple factors, including increased levels of carboxyhemoglobin, atherosclerosis, and vasoconstriction. Subcutaneous tissue oxygen tension begins to decrease 10 minutes after the initiation of cigarette smoking, reaches a low of 22% to 48% below baseline after approximately 30 minutes, and remains below normal for up to 1 hour. The combination of nicotine-mediated vasoconstriction and increased levels of carbon monoxide in smokers results in an estimated 70% decrease in subcutaneous tissue oxygenation in regular smokers.
The presence of oxygen is crucial for effective prevention of infection, and smokers have demonstrated increased susceptibility to a number of bacterial infections, including meningitis, periodontitis, otitis media, and infection of the respiratory and urinary tracts. Reactive oxygen species produced by neutrophils and monocytes are necessary for effective functioning of the immune system, and levels are decreased in smokers. Increased subcutaneous oxygen levels postoperatively result in decreased surgical site infection rates, and smokers quitting smoking 4 to 8 weeks prior to surgery have shown a decreased incidence of surgical site infection. Following spine surgery in 583 patients, smoking status was found to be a significant predictor of complications within the first 30 days.
After fusion with segmental fixation for adult spinal deformity, smoking was found to be a risk factor for adjacent-segment problems; the overall relative risk of reoperation for any reason was 2.59 in smokers, with 25.8% requiring another procedure. Prior to elective general surgery or orthopaedic procedures, smokers randomized to receive smoking cessation counseling and offered nicotine replacement therapy had cessation rates significantly higher than the control group, up to 58%, and significantly lower postoperative complication rates. Cessation had the largest effect on reducing surgical site complications. The number needed to treat to prevent one complication has ranged from three to five patients.
Overall Outcomes
After surgical procedures for isthmic lumbosacral spondylolisthesis or chronic low back pain, smokers were more likely to be dissatisfied and have worse results. Smokers were found to have similar improvements following either surgical or nonoperative treatment for spinal stenosis. Patients actively serving in the military were significantly less likely to return to full-time work following a lumbar microdiscectomy if they were smokers. Twelve months following nonoperative treatment of thoracolumbar compression fractures, smokers were 13% more disabled and 11% less satisfied than nonsmokers.
Musculoskeletal Consequences of Tobacco Use
General Adverse Effects
The remainder of the musculoskeletal system suffers similar consequences due to tobacco use. Smokers experience decreased rates of healing of fractures, fusions, and tissues, which results in poorer outcomes overall and an increased incidence of posttraumatic and postoperative infections. Postoperative smoking predicts failure of fingertip replantations and reduced success of anterior cruciate ligament reconstruction. Following tibial and femoral shaft fractures, smokers are more likely to experience delayed union or nonunion than nonsmokers. A systematic review of fracture healing identified current cigarette use as a risk factor for nonunion of closed fractures, open fractures, and tibial fractures. There was also a trend toward longer fracture healing time and increased infection rate.
Smokers are also at increased risk for rotator cuff tears and are likely to have delayed tendon to bone healing following rotator cuff repair based on findings in a rat model. A causal relationship has also been established between cigarette smoking and the development of rheumatoid arthritis.
Osteoporosis
Smoking has long been associated with the development of osteoporosis and increased risk of fractures. Evidence indicates that smoking is an independent, dose-dependent risk factor for decreased bone density. This finding is not limited to older patients. A study of young male military recruits found smoking to be a risk factor for decreased spine and hip bone mineral density. Research has also shown that smokers have reduced bone size and amounts of cancellous and cortical bone. Estradiol activity is routinely decreased in smokers due to multiple mechanisms. This results in decreased intestinal absorption of calcium and increased risk of osteoporosis. Smoking-related alterations in body mass and composition, estrogen metabolism, calcium absorption, and osteocyte function are thought to have important effects on bone health.
Smoking is believed to increase fracture risk through multiple mechanisms; low bone mineral density cannot account for the entire increase in risk. Effects are seen in both premenopausal and postmenopausal women, although effects are often more significant following menopause and in women with decreased body mass. Men who smoke are also affected and have been found to have a 4% to 15.3% lower bone mineral density than men who had never smoked. Twin studies of same-sex pairs discordant for smoking indicate a possible dose-dependent relationship.
Smokers can have significantly reduced bone mineral density at the lumbar spine, forearm, and calcaneus, with more substantial deficits noted in the hip. Smoking has been shown to increase the lifetime risk of vertebral and hip fractures in both men and women who smoke. Current smoking has also been implicated as a risk factor for proximal humerus and distal forearm fractures. Smokers have been shown to be at risk for sustaining fractures up to 5.2 years earlier than nonsmokers, and fracture risk increased as tobacco consumption increased. Smoking cessation results in a rapid drop in fracture risk during the first 10 years, but the risk of fracture remains elevated for more than 30 years.
There is also evidence that smokers may be more likely to fall than nonsmokers due to relative weakness, poorer balance, and impaired neuromuscular performance. It has been estimated that smokers have the physical and neuromuscular function of someone 5 years older.
Surgical Complications
A review of more than 600,000 patients undergoing major surgery identified current smoking as a risk factor for increased postoperative mortality. Current and, to a lesser degree, past smokers were both more likely to sustain postoperative arterial and respiratory events than never smokers. Smoking cessation at least 1 year before major surgery was found to remove the increased mortality risk. An additional review of more than 520,000 patients verified that smoking is associated with increased perioperative cardiopulmonary, wound, and infection-related complications.
Following total hip arthroplasty, tobacco use was associated with an increased risk of systemic complications, including venous thromboembolisms and acute cardiac or cerebrovascular events. Heavy smokers experienced a 121% increased risk, whereas current and previous smokers had a 56% and 43% increased risk, respectively. A separate review found increased rates of surgical site infections, pneumonia, stroke, and mortality in current smokers following total joint arthroplasty.
Epidemiology of Tobacco Use
Worldwide
Tobacco use, which is linked to 100 million deaths in the 20th century and currently accounts for 6 million deaths and more than half a trillion dollars in economic damages each year, has been classified as an epidemic by the World Health Organization. At current rates, tobacco use will result in more than 8 million deaths a year by the year 2030 and an estimated 1 billion deaths in the 21st century. Tobacco kills one third to one half of all people who use it—one person every 6 seconds—resulting in death approximately 8 to 16 years prematurely. More than 40% of men and approximately 12% of women smoke tobacco worldwide.
In the United States
In the United States, cigarette smoking kills an estimated 480,000 people each year. This is more than the number of people killed as a result of car accidents, alcohol abuse, illegal drug use, homicide, and AIDS combined. Since 1964, more than 20 million Americans have died prematurely due to smoking-related illnesses. At the current rate, 25 million smokers alive today will die due to the adverse effects of smoking. Cigarette-related residential fires result in more than 1000 deaths each year, making cigarettes the number one cause of residential fire fatalities.
The 2013 National Survey on Drug Use and Health found that 66.9 million Americans 12 years of age and older were current tobacco users. As shown in Table 176-3 , a majority of these, 55.8 million, were current cigarette smokers. The rate of tobacco use varies greatly between age groups, with people 18 to 25 years of age having the highest rate of tobacco use in the previous 30 days, 37%. Of youths 12 to 17 years of age, 7.8% had used a tobacco product in the past 30 days.
| Number of People (in millions) | Percentage of U.S. Population | |
|---|---|---|
| Cigarette smokers | 55.8 | 21.3 |
| Cigar smokers | 12.4 | 4.7 |
| Smokeless tobacco users | 8.8 | 3.4 |
| Pipe smokers | 2.3 | 0.9 |
| Any tobacco use | 66.9 | 25.5 |
Financial Costs
The financial burden of tobacco use on society is overwhelming. It is estimated that tobacco use is responsible for $132.5 to $175.9 billion in direct medical costs for the care of adults in the United States each year. An additional burden of $156.6 billion annually can be attributed to lost productivity due to tobacco use. By not fully accounting for other costs associated with tobacco use, such as diseases due to secondhand smoke and burns related to tobacco use, the estimated annual cost associated with tobacco use of $289 to $322.5 billion is likely a significant underestimate.
Secondhand Smoke
Passive, or secondhand, smoke has also been shown to increase the risk of smoking-related illness. It is estimated that approximately 3000 lung cancer deaths and 46,000 deaths from coronary artery disease are due to passive smoke exposure each year. Children exposed to tobacco smoke are at increased risk for sudden infant death syndrome and respiratory and ear infections. In addition, they are more likely to develop asthma and to have more severe symptoms.
Trends of Tobacco Use
As of 1960, approximately 50% of adult men in the United States were cigarette smokers. Since the 1946 release of the surgeon general’s report on smoking and health, increased awareness of the harms of tobacco use have led to an almost 50% decrease in the number of Americans using tobacco ( Fig. 176-1 ). The prevalence of cigarette smoking among adults was estimated to be 21.3% in 2013 compared to 26% in 2002 and 42% in 1965. Between 2000 and 2007, there was an 18% decline in cigarette sales in the United States. The average price of a pack of cigarettes increased from $2.93 to $3.93 during the same period. Although the rate of cigarette use by 18- to 25-year-olds decreased from 40.8% in 2002 to 30.6% in 2013, the rate of smokeless tobacco use increased from 4.8% to 5.8%. The rate of any tobacco use by adults decreased from 30.4% to 25.5% from 2002 to 2013.
In 2007, there were approximately 6100 new cigarette smokers 12 years of age and older every day, for a total of 2.2 million new smokers. Of these, 59.7% were younger than 18 years of age. New smoking rates continue to be high with a reported 2.3 million new smokers in 2012, 52.2% being younger than 18 years of age. In 2013, a higher percentage of males than females (31.1% versus 20.2%) reported tobacco use during the previous 30 days.
There is significant variability in the rate of tobacco use between the different ethnic groups in the United States. In 2013, the prevalence of past month tobacco use in those 18 years of age and older was 10.1% for Asians, 18.8% for Hispanics, 25.8% for Native Hawaiians or other Pacific Islanders, 27.1% for blacks, 27.7% for whites, 31.2% for people reporting two or more races, and 40.1% for American Indians or Alaska Natives. Educational level inversely influences cigarette use, with use decreasing as education increases.
As of 2006, Utah had the lowest smoking rates, with 10.4% of men and 9.3% of women 18 years of age or older reporting current cigarette use. Kentucky had the highest smoking rates, with 29.1% of men and 28% of women, for the same period.
People with mental illness compose one group that has not seen an appreciable decrease in smoking rates. Although smoking rates have been reported near 90% in people with schizophrenia, smoking rates are two to four times greater in people with bipolar disorder, major depression, posttraumatic stress disorder, and other mental illnesses than in the general population. People with psychiatric disorders are believed to purchase more than 40% of cigarettes sold in the United States.
Also associated with increased cigarette use, current illicit drug use was reported in 24.1% of smokers compared with 5.4% of those not currently using cigarettes. Similarly, alcohol use was reported by 65.2% of cigarette smokers compared with 48.7% of nonsmokers. Cigarette users were also more likely to be heavy drinkers and participate in binge drinking than those not currently using cigarettes.
A corresponding increase in sales of other tobacco products negated approximately 30% of the decline in cigarette sales. For example, cigar sales increased by 37% from 2000 to 2007, and use of noncigarette smoked tobacco products, including bidis, kreteks, and shisha, has also increased. Early data suggest that electronic cigarette use by adults was 6.2% in 2012, with the highest rates being seen for current (21.2%) and former (7.4%) cigarette smokers.
Tobacco and Tobacco Smoke
The composition and behavior of tobacco smoke is a complex subject that is not fully understood. The identities, behaviors, and health consequences of many of the components of tobacco smoke have yet to be well defined. Tobacco and tobacco smoke contain approximately 7000 compounds, about 4000 of which have been identified. At least 69 of these compounds are known to be carcinogenic in mammals, and 11 are known to be human carcinogens. An average commercially produced cigarette in the United States is filled with 700 mg of tobacco, which contains 10 to 14 mg of nicotine. Nicotine (C 10 H 14 N 2 , 1-methyl-2-(3-pyridyl)-pyrrolidine) is a naturally occurring plant alkaloid and is responsible for a majority of the addictive properties of tobacco.
Some compounds in tobacco smoke that are considered hazardous include formaldehyde, acetaldehyde, benzene, carbon monoxide, arsenic, isoprene, toluene, acetone, styrene, ammonia, hydrogen cyanide, and vinyl chloride. Almost all of the common elements have been identified in tobacco, including a number of radioactive isotopes and free radicals. Many, including cadmium, mercury, titanium, and lead, are also found in tobacco smoke. When inhaled, tobacco smoke is an aerosol with a gas phase containing approximately 8% particulate material on a weight basis. There are approximately 109 to 1010 particles/cm 3 in tobacco smoke, with 50% to 90% being retained in the lungs after expiration.
Although cigarettes are a roll of tobacco wrapped in a substance not containing tobacco, cigars consist of tobacco wrapped in leaf tobacco or in any substance containing tobacco. Cigar tobacco is high in nitrate, and the fermenting process unique to cigars converts the nitrate to very high levels of carcinogenic nitrogen-containing compounds. Cigar smoke also contains elevated levels of tar, ammonia, nitrosamines, and nitrogen oxides. Having a higher pH than cigarette smoke, cigar smoke contains higher concentrations of free nicotine in the particulate and vapor phases. This is absorbed through the oral mucosa and does not require the cigar to be lit. Some cigars contain as much tar and nicotine as a pack of cigarettes.
Electronic cigarettes (e-cigarettes) deliver a nicotine-containing aerosol by using battery power to heat a propylene glycol based solution. Marketed as a healthier alternative to tobacco smoking and a smoking cessation aid, the adverse effects of e-cigarettes are not yet known and they have not been shown to improve smoking cessation rates. E-cigarettes and solutions are not currently regulated in the United States, resulting in significant variation in solution composition and device performance.
Nicotine
Cigarettes are very efficient means of drug delivery. With typical use, 10 puffs over a 5-minute period, an average smoker receives 1 to 2 mg of nicotine per cigarette. When inhaled, nicotine is quickly absorbed into the venous circulation, avoiding first-pass metabolism and reaching peak concentrations within 10 seconds. With smokeless tobacco and most cigar and pipe use, nicotine levels peak more slowly as the nicotine is absorbed through the mucosal membranes. To facilitate absorption of nicotine, a weak base, through the mucous membranes, chewing tobacco and snuff are buffered to an alkaline pH, near 7 or 8. Peak nicotine concentrations following the use of chewing tobacco are reached in approximately 30 minutes and are maintained for about 2 hours. Air-cured tobaccos, commonly used in pipes and cigars, produce smoke with a relatively alkaline pH, facilitating mucosal absorption of nicotine.
Nicotine distributes throughout the body; plasma levels of nicotine in regular smokers range from 50 nmol/L in light smokers to 300 nmol/L in heavy smokers. Nicotine concentrations in breast milk are approximately three times greater than maternal serum concentrations, and nicotine accumulates in amniotic fluid and fetal tissues.
Specific Adverse Health Effects of Tobacco Use
Cancer
Approximately one third of all cancer deaths can be attributed to smoking, and rates of death from cancer are twice as high in smokers and four times as high in heavy smokers than in nonsmokers. Smoking is linked to 90% of all lung cancer cases, and lung cancer accounts for 80% of cancer deaths attributed to smoking. Other cancers associated with smoking include oropharyngeal, laryngeal, esophageal, stomach, colorectal, pancreatic, cervical, renal, bladder, and acute myelogenous leukemia. Of all possible carcinogens present in tobacco, the seven tobacco-specific nitrosamines have emerged as some of the most active based on rodent and preliminary human studies. Nonsmoking adults living with a smoker have been found to have a 20% to 30% increased risk of lung cancer compared with the general population.
Numerous rodent studies have confirmed the ability of oral snuff to cause oral cancers. Many suspected carcinogens, including the tobacco-specific N -nitrosamines, are present in oral tobacco. Snuff also contains the radioactive isotope polonium-210, formaldehyde, and acetaldehyde.
Although investigators have not shown that nicotine is a direct carcinogen, animal studies suggest that it acts as a tumor promoter by inhibiting apoptosis and preventing the killing of malignant cells. Increased angiogenesis seen in animals receiving nicotine may contribute to tumor growth and eventual metastasis.
Cardiovascular Effects
Cigarette smoking increases the risk of coronary artery disease by 80%. It also increases the incidence of stroke, angina, myocardial infarction, and fatal coronary artery disease. Both primary and secondhand tobacco smoke are associated with the development of atherosclerosis. Passive smoking increases the risk of coronary artery disease by 30% and the risk of stroke by 20% to 30%.
Proposed mechanisms leading to the increased incidence of acute myocardial infarction seen in smokers include increased coronary artery vascular resistance, stimulation of coronary vasospasm, increased risk of plaque rupture or erosion, and induction of thrombosis. Cigarette smoking is associated with decreased availability of nitric oxide, a free radical responsible for initiating vasodilation, especially in the coronary arteries and microvascular beds.
Cigarette smoke has been associated with an increased peripheral blood leukocyte count and increased markers of inflammation, including C-reactive protein, interleukin-6, and tumor necrosis factor alpha. This results in increased leukocyte recruitment, adherence to the endovascular endothelium, and the transendothelial migration of monocytes. The lipid profiles of smokers traditionally show decreased levels of high-density lipoprotein with increased levels of low-density lipoprotein, serum cholesterol, and triglycerides. Platelets from smokers have an increased propensity to aggregate, both spontaneously and following stimulation.
Pulmonary Effects
Cigarette smoke leads to pulmonary emphysema through the initiation of inflammatory responses in lung tissues and impairment of repair processes. Following exposure to cigarette smoke, appropriate recruitment and proliferation of lung fibroblasts and epithelial cells is inhibited. Similarly, cigarette smoke inhibits lysyl oxidase, the enzyme responsible for cross-linking and polymerizing elastin.
Pregnancy
Nicotine easily crosses the placenta and can reach fetal concentrations that are 15% higher than maternal levels. Additionally, elevated levels of maternal and fetal carbon monoxide can decrease fetal oxygen delivery. Adverse outcomes associated with smoking during pregnancy include fetal growth retardation, congenital malformations, decreased birth weight, spontaneous abortion, and sudden infant death. In addition to an estimated 910 infant deaths annually due to smoking, costs due to smoking-related neonatal care are believed to be more than $350 million a year. As a later consequence, children of mothers who smoked more than one pack a day during pregnancy have almost twice the risk of developing nicotine dependence.
Addiction and Dependence
The Diagnostic and Statistic Manual of Mental Disorders-IV (DSM-IV) defines substance dependence as a maladaptive pattern of substance use leading to clinically significant impairment or distress ( Box 176-1 ). Dependence on nicotine is more prevalent than on any other substance of abuse. The most basic explanation of nicotine’s addictive properties, like those of other drugs of abuse, is that it activates reward pathways ( Table 176-4 ).
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