day had three times the risk. Overall, the increased incidence of oropharyngeal cancer in smokers compared with that in nonsmokers across studies ranges from 3 to 13 (Schottenfeld and Fraumeni, 1996).

The most likely causal pathway between tobacco use and these cancers is the direct contact of the carcinogens in tobacco and its smoke with the tissues of the oral cavity, larynx, and esophagus. Yet, although smoking alone is an independent risk factor for oral, laryngeal, and esophageal cancer, alcohol consumption greatly exacerbates smoking’s effect on risk (Blot et al., 1988). It is estimated that alcohol and tobacco use together account for approximately 75 percent of oral cancers in the United States (Blot et al., 1988).

There is convincing evidence that former smokers have lower risks of cancers of the oral cavity, pharynx, larynx, and esophagus than current smokers. For oropharyngeal cancer, the risk for former smokers compared with that for current smokers decreases steadily with the number of years since cessation (after the first few years), with some studies demonstrating that the risk of oropharyngeal cancer actually returns to that for never smokers 10 or more years after quitting (Blot et al., 1988). As with lung cancer and smoking cessation, there is also good evidence that the excess risk of oropharyngeal cancer decreases with younger age at cessation (US DHHS, 1990). For laryngeal and esophageal cancer, numerous studies have demonstrated significant drops in risk for former smokers compared with that for current smokers beginning 3 to 4 years after cessation (US DHHS, 1990).

Tobacco Use and Bladder Cancer

Approximately 56,500 cases of bladder cancer are diagnosed each year (ACS, 2002a). Whites have the highest incidence rates, about twice the rate of Hispanics and African Americans (Miller et al., 1996). Significant disparity in the incidence of bladder cancer also exists by sex, as men are about three to four times more likely to develop the disease than women (Miller et al., 1996).

There is convincing evidence that smoking is a cause of bladder cancer. More than 30 case-control and 10 prospective cohort studies support a strong link between smoking and the disease (Silverman et al., 1992). Overall, moderate to heavy smokers tend to have two to five times the risk of nonsmokers, and there is a strong dose-response relationship between smoking and the risk of bladder cancer, with the risk increasing with the duration and amount of smoking. Specifically, the 40-year analysis of British male doctors found that the rate of mortality from bladder cancer was three times greater among heavy smokers (those who smoke 25 or more cigarettes a day) than among nonsmokers (Doll et al., 1994). The most likely causal pathway between tobacco smoking and bladder cancer is the expo-

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