Smoker’s palate (nicotinic stomatitis) is a reactive change associated primarily with the heat generated by combustible tobacco, more frequently observed in pipe smokers than cigarette smokers. It results in thickening of the mucosa and inflammation of the salivary glands of the palate, causing a grayish-white appearance with reddened spots. Smoker’s melanosis (excess pigmentation of the mucosa) may occur on the attached gingiva as a result of the activation of melanocytes. Although this change may be of esthetic concern, there is no clinical significance attached to the diagnosis. When smoking is discontinued, the condition may reverse. 41 Black hairy tongue is another condition that is associated with smoking. It is a reactive hypertrophy of the papillae of the tongue. It usually resolves upon discontinuing smoking. Other changes Other oral changes associated with tobacco smoking include tobacco stains on the teeth, particularly the lower anterior teeth. Halitosis is also frequently associated with smoking. 41 Secondhand smoke is responsible for 46,000 heart disease deaths and 3,400 lung cancer deaths among nonsmokers each year. 46 One hour of secondhand smoke in an enclosed space generates enough nicotine to reach the brain and bind to receptors in the brain of both smokers and nonsmokers that are normally activated only by direct exposure to tobacco smoke. Exposure to secondhand smoke makes it more difficult for adult smokers to quit. 47 Children exposed to secondhand smoke are at increased risk for acute respiratory infections, middle-ear problems, and more severe asthma. 43 Smoking by parents contributes to bronchitis and pneumonia, increases the risk of ear infections, and slows lung growth in their children. 43 Children who are exposed to secondhand smoke are inhaling many of the same cancer-causing substances and poisons as smokers, and the likelihood of their becoming teenage smokers increases. 47 Because their bodies are still developing, infants and young children are especially vulnerable to the poisons in secondhand smoke. Both infants whose mothers smoke while pregnant and babies who are exposed to secondhand smoke after birth are more likely to die from SIDS than babies who are not exposed to cigarette smoke. 48 contaminated dust and smoke residue. The compounds from thirdhand smoke are stable under indoor conditions, so levels can build up over time and become higher if smoking continues. Those closest to the floor (infants) are at the greatest risk of exposure to the effects of thirdhand smoke. 49
There is an increased association of cancers of the oropharyngeal region with a history of tobacco use. 37 The risk level is related to the amount and duration of smoking. Although tobacco smoke from cigarettes can cause cancers anywhere in the mouth or throat, the most common anatomical sites are the lateral border of the tongue, the floor of the mouth, and the oral pharynx. On presentation, oral cancer may appear as a white, red, or red and white lesions. In later stages there may be ulceration, bleeding, and development of a mass that is firm on palpation. 38,39 However, many oropharyngeal cancers are not palpable. Early symptoms may include difficulty in swallowing or the inability to wear dentures. 38,39 Alcohol consumption alone increases the risk of developing oropharyngeal cancers. Smoking and drinking in combination are synergistic and increase the odds for developing oral cancer. 40 Mucosal changes Secondhand smoke Health risks for nonsmokers are associated with exposure to secondhand smoke. Secondhand smoke is composed of sidestream smoke (the smoke released from the burning end of a cigarette) and exhaled mainstream smoke (the smoke exhaled by the smoker). While secondhand smoke has been referred to as environmental tobacco smoke (ETS) , the term “secondhand smoke” better captures the involuntary nature of the exposure. Secondhand smoke has been classified as a known human carcinogen (cancer-causing agent) by the U.S. Environmental Protection Agency, 42 the National Toxicology Program, 43 and the International Agency for Research on Cancer, 44 and as an occupational carcinogen by the National Institute for Occupational Safety and Health. 45 Secondhand smoke contains many of the same chemicals that are present in the smoke inhaled by smokers. Because sidestream smoke is generated at lower temperatures and under different conditions than mainstream smoke, sidestream smoke contains higher concentrations of many of the toxins in cigarette smoke. The National Toxicology Program estimates that at least 250 chemicals in secondhand smoke are known to be toxic or carcinogenic. 43 Thirdhand smoke The concept of thirdhand smoke is relatively new. Smoke can be converted to potent and carcinogenic substances after it is dissolved on indoor surfaces. The carcinogenic tobacco-specific N-nitrosamines (TSNAs) cling to the smoker’s skin and hair, as well as dust and fabrics. Nonsmokers are at risk via dermal contact and by inhaling
NICOTINE IN COMBUSTIBLE TOBACCO
Physiologic effects of nicotine It is important to note that nicotine itself is not a carcinogen but a chemical that affects the brain and perpetuates tobacco use to avoid the unpleasant physiological symptoms that result from the absence of nicotine. Nicotine satisfies the criteria for drug dependence that include compulsive use, psychoactive effects (affecting the brain), withdrawal, and drug-reinforced behavior. Additional criteria include stereotypical patterns of use, use despite knowledge of harmful effects, relapse during abstinence, and recurrent cravings. Nicotine use produces tolerance or the need for the drug in greater quantities to achieve the same effect. 50
The cigarette is the most effective drug-delivery system available; in fact, it is more effective than intravenous injection. Dr. Richard Hurt of the Mayo Clinic in Rochester, Minnesota, has referred to the cigarette as “the holy grail of drug delivery devices.” 51 When cigarette smoke is inhaled, nicotine is rapidly absorbed into the lungs and enters the blood vessels there. Nicotine is delivered to the brain within ten seconds. Nicotine activates cholinergic neurons in different regions throughout the brain. This stimulation leads to an increased release of acetylcholine from the neurons. Stimulation of cholinergic neurons promotes the release of dopamine in the reward pathways of the brain. Stimulation
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