Smoking tobacco is the single most preventable cause of death and disease in the United States (1). In 2005, smoking tobacco was responsible for 467,000 deaths, accounting for about 1 in 5 deaths in US adults (1). In the United States, an additional 8.6 million people have serious illnesses that are caused by smoking—chronic bronchitis and emphysema account for more than half of them. For every person who dies from tobacco use, another 20 suffer with at least 1 serious tobacco-related illness (2). Tobacco use also represents a huge economic burden. During the time period from 2000 to 2004, cigarette smoking was estimated to be responsible for $96 billion in direct medical costs and $97 billion in lost productivity (3).

Unfortunately, it is estimated that 46 million American adults currently smoke cigarettes (4). Even though the numbers remain high, there has been a significant decrease in cigarette smoking over the last 40 years (5). From 1965 to 2008, the percentage of the US population who smoke decreased from approximately 42% down to 20.6% (4,5). However, this decrease has leveled off over the last 5 years (4). Fortunately, of the estimated 94 million people who have ever smoked, 51.1% have now quit, and since 2002, the number of former smokers outnumbers the number of current smokers (4).

Smoking has historically been more common in men. Centers for Disease Control and Prevention data from 2008 suggest a prevalence of smoking in the United States of 23.1% among men and 18.3% among women. There is also some variability with regard to age. In general, the percentage of smokers 18 to 65 years of age does not vary significantly from the national average—however, there are significantly fewer adults over age 65 who smoke. This age group has a smoking prevalence of only 9.3%.

Tobacco use patterns also vary by socioeconomic status. The prevalence of smoking among adults with a graduate degree is only 5.7%, while the prevalence of smoking is highest among adults who had only earned a General Education Development certificate. This is consistent with data demonstrating that individuals with higher education also have a much higher awareness of the risks associated with smoking (6). Smoking is also much more common in adults living below the poverty level compared to those living above the poverty level, with a prevalence of 31.5% and 19.6%, respectively. Tobacco use is also not uniform between different ethnic groups. Asians have the lowest prevalence at 9.9%, followed by Hispanics at 15.8%, non-Hispanic blacks at 21.3%, non-Hispanic whites at 22.0%, and American Indians the highest at 32.4% (4).

The chemical primarily responsible for tobacco dependence is nicotine. Nicotine is a highly addicting drug. Its main targets in the central nervous system are neuronal nicotinic acetylcholine receptors. It also acts on the mesolimbic dopamine system, resulting in reward signaling and addiction. Its effects on the brain reduce anxiety and relieve stress, in addition to slight cognitive enhancement and increased ability to fight fatigue (7,8). Interestingly, there is a strong genetic component to nicotine dependence (9). The bioavailability of nicotine is around 12% in cigarette smoke, representing an uptake of about 1 mg of nicotine per cigarette. However, this uptake is variable depending on the method used to smoke the cigarette and can be increased to up to 40% bioavailability. It is generally considered that a dose of 5 mg of nicotine per day can result in addiction, but this is variable among individuals. Nicotine is metabolized in the liver and the principal metabolite is cotinine. Cotinine levels in blood, urine, hair, saliva, or nail can be measured and are directly proportional to the amount of nicotine the patient has recently been exposed to. Per cigarette, smokers produce 14 ng of cotinine per milliliter of blood. It is generally considered that a nonsmoker should have 3 ng/mL or less of cotinine in his or her bloodstream (10,11). The clinician can verify cessation of smoking using this test.

Tobacco cessation is a critical part of the patient encounter for the otolaryngologist. Smoking impacts patients in a multitude of ways, and efforts directed toward cessation provide the foundation of preventive medicine for all areas in the field of otolaryngology. In fact, tobacco abuse can lead to decreased olfaction, thyroid disease, rhytids, tooth discoloration, gum disease, cancer, decreased taste, voice changes, sore throat, hearing loss, and many of other conditions. Smoking also increases the rate of postoperative complications and impairs wound healing.

Head and neck cancer is directly caused by tobacco use. Smoking cessation efforts are fundamental to efforts to decrease the incidence of head and neck cancer. Multiple studies conclude that quitting smoking can lower the incidence of second malignant lesions in head and neck cancer patients from 40% down to 5% to 20%. However, this is controversial. Other data suggest that patients who have reached a critical level of damage due to prolonged tobacco exposure will not see this benefit. In this model, it is hypothesized that after a certain level of exposure, the damage caused by tobacco exposure is irreversible, even with cessation. This model also proposes that, for this reason, individuals who have the least amount of tobacco exposure will have the most benefit from cessation (12).

Secondhand smoke also poses a significant health risk. In fact, there is no level of secondhand smoke that is riskfree and the presence of any secondhand smoke carries risk of developing complications. Secondhand smoke has been proven to cause premature death and disease in both children and adults who are nonsmokers. In children, secondhand smoke results in increased risk for sudden infant death syndrome, acute respiratory infections, ear infections, and asthma. Children exposed to smoking by their parents also demonstrate slowed lung growth and suffer from respiratory symptoms. Adults exposed to secondhand smoke can develop coronary artery disease and lung cancer (13).