associated with a higher lung cancer risk (Sidney et al., 1995), although not in other studies of menthol cigarettes (Kabat et al., 1991). In two studies the carbon monoxide (CO) boost was shown to be higher among users of menthol cigarettes (Clark et al., 1996; Jarvik et al., 1994), but not in another study that examined women (Ahijevych et al., 1996). Another mechanism for potential harm from mentholation is pyrolysis of menthol, which leads to benzo[a]pyrene production (Schmeltz and Schlotzhauer, 1968). Socioeconomic status may also contribute to racial differences in lung cancer incidence (McWhorter et al., 1989).
African Americans tend to smoke less than Caucasians (Hahn et al., 1990; Kabat et al., 1991; Royce et al., 1993; Vander Martin et al., 1990), but may be more highly nicotine dependent (Royce et al., 1993; Vander Martin et al., 1990). They also tend to smoke higher-tar and nicotine cigarettes, resulting in higher nicotine levels and greater tar yields (Hahn et al., 1990; Perez-Stable et al., 1998). This is consistent with repeated findings of higher cotinine levels in African Americans compared to Caucasians (Caraballo et al., 1998; Wagenknecht et al., 1990) and higher urinary TSNAs in African Americans (Richie et al., 1997). Even though it was recently shown that African Americans have decreased cotinine clearance, rather than different nicotine metabolism (Perez-Stable et al., 1998), there is still the possibility of higher relative carcinogen exposure. For example, this study did not consider smoking topography. There are data showing that African Americans smoke more of their cigarettes (Clark et al., 1996) and have a higher CO boost per millimeter of cigarette smoked (Ahijevych et al., 1996; Clark et al., 1996). They also have higher nicotine intake per cigarette (Perez-Stable et al., 1998).
When considering a PREP, we must consider different races within the United States and other countries, where more environmental exposures are shared. In general, within levels of smoking, the risks of lung cancer around the world are similar, with some exceptions. In China, a combined analysis of studies that appeared in the Chinese literature reportedly demonstrated a dose-response relationship for men and women (Liu, 1992). However, the slope of the dose-response relationship was less than that in Western studies and similar to that for Japan. Importantly, the attributable risk for smoking was only 57% in men and 26% in women, where 88% and 46% of male and females smoked, respectively. A substantial number of Chinese also smoked pipes of various types, and among these individuals, the risk of lung cancer was lower than among persons who smoked only cigarettes (Lubin et al., 1992). Whether this represents a method of harm reduction remains unknown since that was not specifically studied, and the lower risk might have been observed for many reasons. Caution must be used in attempting to implicate any particular factor for differences in lung cancer rates in different geographical