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Warm Springs (OR): Warm Springs Confederated Tribes, Community Health Promotion Department, Human Services Branch, 1993. 134 Chapter 2 Chapter 3 Health Consequences of Tobacco Use Among Four Racial/Ethnic Minority Groups Introduction 137 Lung Cancer 137 African Americans 138 American Indians and Alaska Natives 143 Asian Americans and Pacific Islanders 1 J.5 Hispanics 147 Other Cancers 149 Cervical Cancer 252 Esophageal Cancer 2.53 Oral Cancer 153 Stomach Cancer 155 Urinary Bladder Cancer 156 Chronic Obstructive Pulmonary Disease 158 African Americans 158 American Indians and Alaska Natives 158 Asian Americans and Pacific Islanders 159 Hispanics 159 Coronary Heart Disease 160 African Americans 160 American Indians and Alaska Natives 161 Asian Americans and Pacific Islanders 2 62 Hispanics 163 Cerebrovascular Disease 164 African Americans 165 American Indians and Alaska Natives 165 Asian Americans and Pacific Islanders 165 Hispanics 166 Smoking and Pregnancy 266 Studies of Low Birth Weight 167 Studies of Infant Mortality and Sudden Infant Death Syndrome 169 Health Problems Affecting Pregnant Women 171 Implications 172 Summary of Health Consequences from Active Cigarette Smoking 172 Effects of Exposure to Environmental Tobacco Smoke 172 Effects of Smokeless Tobacco Use 274 Nicotine Addiction and Racial/Ethnic Differences 175 Nature of Addiction 175 Pharmacologic Factors in Nicotine Addiction 175 Absorption, Distribution, and Elimination of Nicotine in the Body 175 Pharmacodynamics of Nicotine 2 76 Tolerance, Withdrawal, and Addictive Tobacco Use 178 Level of Addiction 179 Racial/Ethnic Differences in Nicotine Metabolites 179 Racial/Ethnic Differences in Self-Reported Nicotine Dependence 281 Racial/Ethnic Differences in Quitting Smoking 283 Addiction to Smokeless Tobacco 183 Conclusions 185 Appendix. Methodological Issues 185 Classification of Smoking Status 285 Classification of Race/Ethnicity 186 Classification of Health Outcomes 287 References 188 Tobacco Use Among U.S. Racial/Ethnic Minority Groups Introduction The fact that cigarette smoking causes cancer, respiratory and cardiovascular diseases, and adverse pregnancy outcomes is well established (U.S. Depart- ment of Health and Human Services [USDHHSI 1989b). Evidence of the relationship between smok- ing and lung cancer began to accumulate as early as the late 1930s (Ochsner and DeBakey 1939; U.S. De- partment of Health, Education, and Welfare [USDHEW] 1964). In 1964, the first Surgeon General's report linking smoking to disease concluded that ciga- rette smoking was a cause of lung and laryngeal can- cers in men and a probable cause of lung cancer in women. In more recent reports, the Surgeon General has concluded that cigarette smoking causes 87 per- cent of lung cancer deaths, 30 percent of all cancer deaths, 82 percent of chronic obstructive pulmonary disease (COPD) deaths, 21 percent of coronary heart disease (CHD) deaths, and 18 percent of deaths from stroke (USDHHS 1989b) as well as 21-39 percent of low-birth-weight births and 14 percent of preterm de- liveries (USDHHS 1980, 1989b). In addition, passive or involuntary smoking causes lung cancer in healthy nonsmokers and respiratory problems in young chil- dren (USDHHS 1986a; U.S. Environmental Protection Agency 1992). Despite this wealth of knowledge about the health consequences of smoking, few studies have Lung Cancer examined the relationship between tobacco use and known health effects among racial/ethnic groups in the United States. Moreover, few databases include information on sufficient numbers of persons from racial/ethnic groups to allow such analyses. Although sufficient data are often not available for these population subgroups, the objectives of this chapter are to assess the burden of smoking-related diseases among U.S. racial/ethnic groups, to examine racial/ethnic differences in tobacco-related morbidity and mortality when possible, and to review studies that have examined how the relationship between to- bacco use and selected health outcomes may differ among racial/ethnic groups. For many of the adverse health outcomes and diseases presented in this chap- ter, smoking is one of many contributing factors. The focus in this chapter is on the disease burden related to smoking among four U.S. racial/ethnic minority groups (African Americans, American Indians and Alaska Natives, Asian Americans and Pacific Island- ers, and Hispanics); data on the contribution of cigarette smoking to any differences between groups are highlighted whenever available. A discussion of some relevant methodological issues is provided in the chapter appendix. The 1964 Surgeon General's report on smoking and health concluded that "Cigarette smoking is caus- ally related to lung cancer in men; the magnitude of the effect far outweighs all other factors. The data for women, though less extensive, point in the same di- rection" (USDHEW 1964). That conclusion was based on strong epidemiological evidence from case-control and cohort studies and supporting toxicological evi- dence. When reviewed against criteria for causality, the evidence was initially judged to be sufficient for men and a similar conclusion was subsequently reached for women (USDHHS 1980). Since the 1964 Surgeon General's report, voluminous evidence has accumulated about the relationship between smoking and lung cancer (USDHHS 1989b; Wu-Williams and Samet 1994). The epidemiological studies consistently indicate that the risk of lung cancer increases with the number of ciga- rettes smoked and with the length of time a person smokes. Furthermore, evidence shows that in com- parison with smokers of non-filtered cigarettes, smok- ers of filtered cigarettes have only slightly less risk of lung cancer (Wu-Williams and Samet 1994). Although a family history of lung cancer is associated with in- creased risk, the genetic basis for this association has not yet been determined (Economou et al. 1994). En- vironmental agents other than cigarette smoke, includ- ing certain occupational agents (Coultas and Samet Health Coilseqzlel7ccs 237 Suqeon General's Report 1992; Coultas 1994) and indoor and outdoor air pol- lutants (Samet 1993), also cause lung cancer. For ex- ample, synergism between smoking and radon and asbestos has been demonstrated in studies of worker groups (Saracci and Boffetta 1994). Because nearly all cases of lung cancer are attrib- utable to cigarette smoking, variations in lung cancer patterns between racial/ethnic groups most likely re- flect differences in smoking patterns. Whenever more detailed information is available, it is included in the appropriate sections that follow. African Americans The population-based cancer registries operated by the National Cancer Institute's (NC11 Surveillance, Epidemiology, and End Results (SEER) Program pro- vide cancer incidence data for several locations throughout the United States, including Connecticut, Hawaii, Iowa, New Mexico, and Utah and the met- ropolitan areas of Detroit, Atlanta, San Francisco/ Oakland, and Seattle/Puget Sound. SEER data show that African American men have had consistently higher lung cancer incidence rates than white men since the 1970s (Figure 1) (Kosary et al. 1995). (SEER data cover about 10 percent of the U.S. population and are used frequently to estimate national cancer rates and trends.) Between 1950 and 1960, age-adjusted death rates for malignant neoplasms of the respiratory system (composed primarily of deaths from lung can- cer) among African American men surpassed those among white men and have since remained higher, whereas death rates for African American women have remained fairly similar to those among white women, according to data from the National Vital Statistics System (Table 1) (National Center for Health Statistics [NCHSI 1997). Since 1990, respiratory cancer death rates declined substantially for African American men; among African American women, rates increased through 1990 and then leveled off. From 1992-1994, the age-adjusted death rate for cancer of the trachea, bronchus, and lung (generally referred to as lung Figure 1. Incidence of cancer of the lung and bronchus, by race/ethnicity and gender, National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program, 1973-1994 10 0 I I I I I I I I I I I 1974 1976 1978 1980 1982 1984 1986 1988 1990 1992 1994 Year of Diagnosis - African American men - a- n * * White men African American women - White women Note: Age-adjusted to the 1970 standard U.S. population. Sources: Adapted from Kosary et al. 1995: Ries et al. 1997. 338 Chapter 3 Tobacco Use Arnmg U.S. Racial/Efhnic Minority Group Table 1. Death rates uer 100,000 U.S. residents for malignant diseases of the respiratory system, by race/ ethnicity a& gender, United States, 1950-1995: selected years - Race/ethnicity and gender African American men All ages, age-adjusted All ages, crude American Indian or Alaska Native men' All ages, age-adjusted All ages, crude Asian American or Pacific Islander men5 All ages, age-adjusted All ages, crude Hispanic men' All ages, age-adjusted All ages, crude White men All ages, age-adjusted All ages, crude African American women All ages, age-adjusted All ages, crude American Indian or Alaska Native women' All ages, age-adjusted All ages, crude Asian American or Pacific Islander women5 All ages, age-adjusted All ages, crude Hispanic women' All ages, age-adjusted All ages, crude White women All ages, age-adjusted All ages, crude 1950+ 1960+ 1970 1980 1985 1990 1992 1993 1994 1995 16.9 36.6 60.8 82.0 87.7 91.0 86.7 86.0 82.8 80.5 14.3 31.1 51.2 70.8 75.5 77.8 74.7 74.7 72.5 71.2 NA NA NA 23.2 28.4 29.7 31.7 31.0 31.1 32.7 NA NA NA 15.7 19.6 21.1 23.1 23.1 23.0 25.1 NA NA NA 27.6 26.9 26.8 27.4 28.4 28.0 25.8 NA NA NA 22.9 21.3 21.7 23.0 23.8 23.9 22.4 NA NA KA NA 24.0 27.7 24.4 25.1 24.8 25.2 NA NA NA NA 13.9 17.4 15.9 16.5 16.5 16.9 21.6 34.6 49.9 58.0 58.7 59.0 56.7 56.3 54.8 53.7 24.1 39.6 58.3 73.4 77.6 81.0 79.5 79.7 78.5 77.8 4.1 5.5 10.9 19.5 22.8 27.5 28.5 27.3 27.7 27.8 3.4 4.9 10.1 19.3 23.5 29.2 30.9 30.2 30.8 31.3 NA NA NA 8.1 11.1 13.5 15.5 16.1 17.7 16.4 NA NA NA 6.4 9.2 11.3 13.4 14.6 16.5 15.5 NA NA NA 9.5 9.2 11.3 11.1 11.7 11.2 13.0 NA NA NA 8.4 8.2 10.6 11.1 11.7 11.4 13.6 NA NA NA NA 6.7 8.7 8.4 8.2 8.5 8.2 5.2 7.5 7.5 7.3 7.7 7.5 4.6 5.1 5.4 6.4 z:: 10.1 13.1 18.2 22.7 26.5 27.4 27.6 27.7 27.9 26.5 34.8 43.4 46.2 47.3 47.9 48.9 - Note: Data in the table on African Americans, American Indians and Alaska Natives, Asian Americans and Pacific Islanders, and whites include persons of Hispanic and non-Hispanic origin. Conversely, in this table, the data on Hispanic origin may include persons of any race. *Age-adjusted to the 1940 U.S. standard population. Cause-of-death data are based on classifications from the then-current Internntio~~al Classification @Diseases (e.g., cause-of-death codes 160-165 for the Ninth Revision). Data for the 1980s are based on intercensal population estimates. `Includes deaths of nonresidents of the United States, tmterpretation of trends should consider that population estimates for American Indians and Alaska Natives increased by 45 percent between 1980 and 1990 (because of better enumeration techniques in 1990 and an _ increased tendency for people to denote themselves as American Indian in 1990). %terpretation of trends should consider that the Asian population in the United States more than doubled between 1980 and 1990, primarily because of immigration. `Because of incomplete data, the National Center for Health Statistics (NCHS) reports 1985 death certificate data on decedents of Hispanic origin for only 17 states and the District of Columbia. By 1990, data for 47 states and the District of Columbia were reported. NCHS estimates that the 1990 reporting area encompassed 99.6 percent of the U.S. Hispanic population. After 1992, only Oklahoma did not provide information on Hispanic origin. NA = data not available. Source: Adapted from National Center for Health Statistics 1997. i,,nzer) WFas highest for African American men (81.6 per I r)(),oOo population) (Table 2); the lung cancer death r,lte for African American women (27.2 per 100,000) ,,.db bimilar to that for white women (27.9 per 100,000) ,),,d ljigher than that for any other racial/ethnic group. .\mc,n~ African Americans in 1993, the four leading ic1Llse5 of cancer death were lung cancer (26.1 percent (,I ;1l1 cancer deaths), cancer of the colon and rectum ( 10.4 percent), prostate cancer (9.4 percent), and can- ik'T ()f the female breast (8.3 percent) (Parker et al. 1997). The higher lung cancer incidence and death rates ~,mo~~g African American men have not been fully ex- pl,lined. Two ecological analyses of population-based in ,lccounted for the differences in lung cancer be- t\\.ct'n white and African American men, whereas the ,luthors of the other paper (Devesa and Diamond 1983) pr~~posed that cigarette smoking and other environ- tnctntal correlates of socioeconomic status, such as dietary habits or occupational exposure, may have .licounted for their findings. Data from several National Health Interview `;url-cvs (NHISs) were used to conduct birth cohort ,~n,>lyll~~\~ et al. 1991; Shopland 1995). Older white men (tho5; born before 1915) experienced higher peak \nloking rates and slightly earlier ages of initiation th,ln older African American men. For persons born ,litc>r 1915, peak smoking rates and duration of smok- ing tor African American men were slightly higher than those> ior white men. In addition, Lvhite male smokers \\`c'rt' more likely than African American male smok- l'r\ to quit smoking in the 1950s (when the early ~it~tific studies on smoking and lung cancer were n~p~~rted); African American male cohorts born after IL) 15 thus experienced a greater cumulative exposure 10 cl$lrette smoke. Reflecting these trends in smok- Ills bc+avior, lung cancer mortality rates were initially ill&t>r for white men. The combination of less cessa- tl~)n, ljigher peak prevalence, and longer duration (`1 \moking in African American men after the 1940s Ilhc'l\' cl\plains the observation that mortality rates for -\trl~-cln American men began to exceed those for white 1111'1J Illttlr in the century (Shopland 1995). Lung cancer death rates have been much lower for women than for men (reflecting historically lower smoking prevalences) and have risen more slowly with age in the older birth cohorts. As rates for men began to decline in cohorts born after 1930, rates continued to rise among women, reflecting their slower adop- tion and increasing prevalence of cigarette smoking. African American and white women indicated simi- lar patterns of smoking initiation, maintenance, and quitting; lung cancer death rates for African Ameri- can and white women also have been similar (Tolley et al. 1991; Shopland 1995). These data are consistent with the interpretation that trends in smoking behav- ior are largely responsible for 20th century lung can- cer mortality patterns for African Americans and whites. Tolley and colleagues (1991) further suggested that lung cancer rates among African American men and women may be slightly higher than those for white men and women, even after considering differences in their smoking behaviors. One study (Harris et al. 1993) showed a higher lung cancer risk among African Americans compared with whites who had the same level of cumulative exposure to cigarette smoking. In this 20-year case- control study, 2,678 cases of lung cancer were identi- fied among white men, 238 cases among African American men, 1,394 cases among white women, and 113 among African American women; after adjusting the data for cumulative tar consumption and educa- tion, the researchers found that African Americans had a significantly higher risk of lung cancer. One limita- tion of this study is that it uses the Federal Trade Commission's (FTC's) estimates of tar yield to calcu- late cumulative tar consumption. The ETC's machines are set to parameters that have not changed for de- cades. Because humans smoke cigarettes differently than the machines used by the FTC, the validity of these measures has been called into question (NC1 1996a). In the Kaiser Permanente cohort study, the relative risks of lung cancer were approximately the same for African Americans and whites (Friedman et al. 1997). Dorgan and colleagues (1993) conducted a case-control study to assess race and gender differences in lung cancer, categorizing participants according to consumption of fruits and vegetables. Lung cancer risk was significantly increased for African Americans who currently smoked (compared with never smok- ers and former light smokers), regardless of the amount of vegetables consumed. These analyses were statisti- cally adjusted for gender, age, education, occupation, passive smoking, and study phase. In a recent population-based case-control study to compare the risks of lung cancer for African 73bncco USC Amo~~g U.S. Raczhl/Ethic Minority Groups Table 2. Age-adjusted death rates* for selected smoking-related causes of death, by race/ethnicity and gender, United States, 1992-1994 Disease Category UCD-9 code)+ African American Indian/ Asian American/ American Alaska Native Pacific Islander White Hispanic Men Women Men Women Men Women Men Women Men Women Cancer Lip, oral cavity, pharynx (140-l 49) 7.7 Esophagus (150) 11.4 Stomach (151) 9.5 Pancreas (157) 11.1 Larynx (161) 4.6 Trachea, bronchus, lung (162) 81.6 Cervix uteri (180) NA Bladder (188) 3.2 Kidney, other, unspecified urinary organs (189) 4.3 Cardiovascular diseases Coronary heart disease (410414) 138.3 Cerebrovascular disease (430438) 53.1 Respiratory diseases Bronchitis, emphysema (491492) 4.7 Chronic airway obstruction, not elsewhere classified (496) 17.6 1.8 2.6 1.0 3.3 1.0 3.0 1.2 2.4 0.5 3.0 3.2 0.5 2.7 0.5 4.4 0.9 2.8 0.4 4.1 4.9 2.6 8.9 5.1 3.9 1.7 6.2 3.1 8.1 3.4 3.0 5.5 3.9 7.3 5.2 5.1 3.8 0.8 0.9 0.3 0.6 0.1 1.7 0.4 1.3 0.2 27.2 33.5 18.4 27.9 11.4 54.9 27.9 23.1 7.7 5.7 NA 3.0 NA 2.5 NA 2.2 NA 3.2 1.6 1.2 0.5 1.5 0.6 3.9 1.1 1.8 0.6 2.0 4.4 2.3 1.8 0.8 4.1 1.9 3.1 1.3 85.0 100.4 71.7 36.2 132.5 62.9 82.7 43.9 40.6 23.9 45.9 21.1 1.9 9.0 29.3 22.4 26.3 22.6 22.7 16.3 1.6 2.8 2.9 0.9 6.2 3.8 2.4 6.6 14.2 7.9 2.6 20.4 12.2 8.2 0.9 3.7 *Per 100,000, age-adjusted to the 1940 U.S. standard population. Estimates for Hispanics exclude data from New Hampshire for 1992 and from Oklahoma for 1992-1994. +I&rrzntiolzal Clnssificntim of Discans~s, Ninth Rcz~isio~~, World Health Organization 1977. NA = data not available. Sources: National Center for Health Statistics, public use data tapes, 1992-1994; U.S. Bureau of the Census 1997. Americans and whites across categories of cigarette Surveillance System, a participant in the NCI's SEER smoking status, Schwartz and Swanson (1997) exam- Program. The analyses were stratified by gender and ined incident cases from the Occupational Cancer statistically adjusted for age, education, and cigarette Incidence Surveillance Study. This study operates in smoking behaviors. The overall risks of lung cancer conjunction with the Metropolitan Detroit Cancer (of all histological types) were similar for African Health Comrqzremes 142 Americans and whites. Thus, race did not appear to be an independent predictor of lung cancer in the population as a whole. Howelrer, African Americans were more likely than whites to have developed squa- mous cell carcinoma. Additionally, African American men aged 40-54 years were 24 times more likely than white men of the same ages to have developed lung cancer (of several histological types). The authors con- cluded that the increased risks among younger African Americans may suggest a greater degree of susceptibility to lung carcinogens or greater exposure to other unidentified carcinogens and they called for further research on the topic. Investigators have postulated that the more frequent smoking of menthol cigarettes by African Americans, compared with whites, contributes to their increased rate of lung cancer (Harris et al. 1993). In a recent experimental study of 12 persons after the amount of menthol injected into experimental ciga- rettes was increased, the amount of carbon monoxide exhaled by African American smokers also increased (Miller et al. 1994). In a comparison of smoking be- havior associated with mentholated cigarettes and regular cigarettes among 29 subjects, McCarthy and colleagues (1995) found higher mean puff volume and higher puff frequency after participants smoked regu- lar cigarettes than after they smoked mentholated cigarettes; however, no differences in mean expired carbon monoxide levels were found. A\Tailable data suggest that mentholated cigarettes are not smoked more intensely than regular cigarettes (Jarlik et al. 1994; Miller et al. 1994; McCarthy et al. 1995; Ahijevych et al. 1996). Thus, mentholated cigarettes may pro- mote lung permeability and diffusibility of smoke con- stituents (Jarvik et al. 1994; McCarthy et al. 1995; Clark et al. 1996a). Recent studies have examined the possible role of genetics in determining the risk of lung cancer among African Americans. Crofts and colleagues (1993) identified a restriction fragment length polymor- phism (RFLP) in the gene (CYPIAI) that encodes the enzyme responsible for initiating metabolism of polyaromatic hydrocarbon compounds found in ciga- rette smoke (Guengerich 1992, 1993). In one study of African Americans, the risk of adenocarcinoma of the lung was higher for smokers with the CYPlAl RFLP than for smokers who did not have this RFLP (Taioli et al. 1995). Two other studies, however, did not find an association between the presence of the variant al- lele in African Americans and increased lung cancer risk (Kelsey et al. 1994; London et al. 1995). Taioli and colleagues (1995) also found that persons who had adenocarcinoma with the African American CYPZAI RFLP had lower lifetime cigarette consumption, as measured by pack-years, compared with those who had adenocarcinoma without the polymorphism. However, using a cutoff point of 35 pack-years, London and colleagues (199.5) found no association between the variant CYPZAI variant allele and lung cancer risk based on smoking history. Additionally, a homozygous rare CYPlAl allele associated with the risk of lung cancer among persons from Japan (Kawajiri et al. 1990) was found more often in African Americans than in whites (Shields et al. 1993). How- ever, in a small case-control study, no association was observed between the presence of this polymorphism and lung cancer risk (Shields et al. 1993). Despite strong research interest in this area, scientists have been unable to consistently associate variant alleles with lung cancer susceptibility. The fre- quencies of the polymorphisms of interest appear to be low in United States populations studied thus far. Low frequencies of the alleles of interest suggest that future investigations must allow for an adequate sample size of the group under study and adjustment for factors such as smoking history and age. In addi- tion, low frequency allelic affects may be negated or obscured by high tobacco exposure levels. Two phenotypes were identified in African American and white persons representing poor and extensive extremes of glucuronidation (Richie et al. 1997). Glucuronidation is considered a detoxification pathway because it increases the water solubility of a chemical substrate and facilitates excretion (Goldstein and Faletto 1993). The ratio of conjugated metabolite to free metabolite of a tobacco-specific nitrosamine was 30 percent higher in the urine of white smokers than in African American smokers. This finding suggests that African Americans are at higher risk from nitrosamine exposure during smoking because of a decreased capacity to detoxify carcinogenic tobacco-specific nitrosamines. Hence, variability in glucuronosyltransferase activity, or in clearance of glu- curonide conjugates, may represent another determi- nant of cancer risk. The genetically determined poor, intermediate, or enhanced debrisoquine metabolizer phenotype has been investigated as a risk factor for lung cancer. Homozygous dominant (extensive metabolizer) indi- viduals were found more frequently among white lung cancer patients who smoked cigarettes than white control patients with COPD who smoked cigarettes (Ayes11 et al. 1984). Caporaso and colleagues confirmed the association between the extensive debrisoquine metabolizer phenotype and lung cancer risk. In this study, almost equivalent numbers of extensive metabolizers were found among African Americans (74 percent) and whites (73 percent) (Caporaso et al. 1990). Another approach in assessing the possible role of genetics is using chromosome breaks to measure cancer susceptibility. One research group has devel- oped an in vitro cytogenic assay that measures mutagen-induced chromosome breaks in short-term lymphocyte cultures. This approach has shown a relationship between mutagen sensitivity and elevated lung cancer. However, attempts to use this method as a predictive marker of racial/ethnic differences in can- cer risk in African and Mexican Americans produced inconsistent results (Spitz et al. 1995; Strom et al. 1995; Wu et al. 1996). Carcinogenesis can in\Tolve genotoxic mecha- nisms whereby chemical interactions at critical cellu- lar sites go unrepaired. Alterations in certain genes, kno\vn as proto-oncogenes and tumor suppressor genes, are linked with cancer risk (Land et al. 1983; Marshall et al. 1984; Slamon et al. 1984; Klein and Klein 1985; Denissenko et al. 1996). Some gene alleles that are e\,aluated as markers of lung cancer risk Ivary in their distributions among African Americans and whites. For example, in a study of lung cancer cases and trauma victim controls, Weston and colleagues (1991) found rare Ha-ras-1 alleles more often in the lung tissue of African Americans (17 percent) than in whites (5 percent). For both groups, the prevalence of rare alleles among lung cancer patients was higher than among controls (23 percent for African American lung cancer cases, 15 percent for African American trauma victim controls, 6 percent for white lung cancer cases, and 2 percent for white trauma victim controls). These findings were confirmed in a second study (Weston et al. 1992). African American and white differences in distribution of alleles at the L-myc locus and ~53 genotype have also been reported. The authors con- cluded that L-myc genotypes and p53 variants do not predict lung cancer risk (Weston et al. 1992). In summary, the higher rates of lung cancer ob- served among African American men are consistent with historical patterns of cigarette smoking in this century (Shopland 1995). In addition, African Ameri- can men aged 40-54 years may be especially suscep- tible to lung carcinogens (Schwartz and Swanson 1997), perhaps because they detoxify them differently (Richie et al. 1997). A genetic role in racial and ethnic-specific risk for lung cancer cannot be ruled out, because some studies have shown that African American populations have increased frequencies of rare alleles associated with greater risks for developing lung cancer than whites. However, because of the low frequency of these alleles in the populations under study and the possibility of misclassification bias, studies have been inconclusive (Shields et al. 1993; Taioli et al. 1995). Further, African American smokers prefer mentholated cigarettes, and menthol may promote the absorption and diffusion of tobacco smoke constituents (Jarvik et al. 1994; McCarthy et al. 1995; Clark et al. 1996a). This hypothesis has received inconsistent support in the epidemiological literature. Kabat and Herbert (1991) found no relationship between menthol use and lung cancer risk; however, Sidney and colleagues (1995) suggested that smoking mentholated cigarettes in- creased the risk of lung cancer only in male smokers. Further research could clarify the nature of individual susceptibility and the possible role of mentholation. Reduction in cigarette smoking will undoubtedly lead to reduction in the risk of lung cancer for African Americans. American Indians and Alaska Natives Since the early 19OOs, many studies have docu- mented the low overall occurrence of cancer among American Indians compared with whites (Hoffman 1928; Smith et al. 1956; Smith 1957; Salsbury et al. 1959; Sievers and Cohen 1961; Kravetz 1964; Reichenbach 1967; Creagan and Fraumeni 1972; Dunham et al. 1973; Blot et al. 1975; Lanier et al. 1976; Samet et al. 1980, 1988b; Sorem 1985; Mahoney and Michalek 1991; Nut- ting et al. 1993). Investigations of lung cancer inci- dence and deaths have confirmed that lung cancer is less frequent among American Indians overall than among whites (Coultas et al. 1994). Between 1992 and 1994, age-adjusted death rates for lung cancer per 100,000 among American Indian and Alaska Native men (33.5) and women (18.4) were slightly higher than those among Asian American and Pacific Islanders as well as Hispanics, whereas they were lower than rates among African Americans and whites (Table 2) (NCHS, public use data tapes, 1992-1994; U.S. Bureau of the Census 1997). Mortality rates for malignant diseases of the respiratory system increased from 1980 through 1995 among American Indians and Alaska Natives (Table 1) (NCHS 1997). Nationally, lung cancer is the leading cause of cancer death among American Indians and Alaska Natives. Among those who died of cancer in 1993, the four leading causes of death were lung cancer (26.8 percent), cancer of the colon and rectum (8.9 percent), cancer of the female breast (6.3 percent), and prostate cancer (6.0 percent) (Parker et al. 1997). Additionally, lung cancer was the leading cause of cancer death among both men and women in 10 of the 12 Indian Figure 2. Age-adjusted lung cancer death rates among American Indian and Alaska Native men in seiecteh states compared with rates among all U.S. men, 1968-1987* 80 1 60 - All U.S. men - m - 1. Alaska North Dakota, 111 South Dakota, and Montana Michigan, m--a Minnesota, and Wisconsin - Oklahoma Arizona and New Mexico 1968-l 972 1973-l 977 Years 1978-1982 1983-1987 *Rates presented here were determined using midpoint population estimates for each 5-year time interval and were adjusted to the 1970 U.S. standard population. Source: Valway 1992. Health Service (IHS) areas (Arizona and New Mexico had low rates of lung cancer deaths) (Valway 19921. Lung cancer death rates among American Indians and Alaska Natives have been rising in most IHS areas (Fig- ures 2 and 3) (Valway 1992); national death rates from malignant diseases of the respiratory system have also been increasing (Table 1). Lung cancer death rates vary by IHS area. Spe- cifically, American Indians in the Southwest have had the lowest lung cancer death rates, whereas American Indians in Alaska, North Dakota, South Dakota, and Montana have had rates nearly as high as those in the general U.S. population (Table 3, Figures 2 and 3) (Valway 1992). These differences are associated with variations in smoking among American Indians and Alaska Natives (Centers for Disease Control [CDC] 1987; Welty et al. 1993). In an analysis of data from the 1985-1988 Behavioral Risk Factor Surveillance System (BRFSS) on 1,055 American Indians, Sugarman and colleagues (1992) determined smoking prevalence for three groups of states that contained three specific IHS areas. In this study, the Plains states (Iowa, Minne- sota, Montana, Nebraska, North Dakota, South Dakota, and Wisconsin) contained the Aberdeen, Bemidji, and Billings IHS areas; the West Coast states (California, Idaho, and Washington) contained the Portland and California IHS areas; and the Southwest states (Arizona, New Mexico, and Utah) contained the Al- buquerque, Navajo, Tucson, and Phoenix IHS areas. Cigarette smoking prevalence rates were highest in the Plains states (48.4 percent for men and 57.3 percent for women), intermediate in the West Coast states (25.2 percent for men and 31.6 percent for women), and low- est in the Southwestern states (18.1 percent for men and 14.7 percent for women). These general geo- graphic patterns of smoking prevalence paralleled patterns of lung cancer mortality (Table 3) (Valway 1992). The smoking prevalence estimates from the 1985-1988 BRFSS analyses may be imprecise because of relatively small samples. However, other analyses (American Indians and Alaska Natives, in Chapter 2; Welty et al. 1995) show similar patterns. Another TO~CCCJ USC Amng U.S. Racial/Efhnic Minorify Groups Figure 3. Age-adjusted lung cancer death rates among American Indian and Alaska Native women in selected states compared with rates among all U.S. women, 196%1987* a *, I II All U.S. women Alaska North Dakota, South Dakota, and Montana Michigan, Minnesota, and Wisconsin Oklahoma Arizona and New Mexico I I I I I I I I I I I I I I I 1968-1972 1973-1977 1978-1982 1983-1987 Years *Rates presented here were determined using midpoint population estimates for each S-year time interval and were adjusted to the 1970 U.S. standard population Source: Valway 1992. potential limitation is that American Indians living in the California and Portland IHS areas may be more likely than American Indians from other IHS areas to be misclassified on death certificates as being of other racial/ethnic categories (Valway 1992), suggesting that death rates for American Indians may be underesti- mated in these areas (Sorlie et al. 1992). Lanier and colleagues (1996) recently reported on lung cancer incidence rates for Alaska Native men and women. Lung cancer incidence was higher for Alaska Natives than it was for the general U.S. population. In addition, lung cancer was the most common inci- dent cancer among men and the third most common incident cancer among women (after breast cancer and cancer of the colon/rectum). Lung cancer incidence increased substantially among Alaska Native men (by 93 percent) and women (by 241 percent) between 1969-1973 and 1989-1993. The authors concluded, "Reduction in tobacco use would result in the greatest decreases in cancer rates in this population" (p. 751). Asian Americans and Pacific Islanders Two issues should always be kept in mind when interpreting data about the health consequences of cigarette smoking among Asian Americans and Pacific Islanders: the diversity of this group and the paucity of data. The Asian American and Pacific Islander population of the United States includes approxi- mately 32 national and racial/ethnic groups and nearly 500 languages and dialects. Although many of these persons were born in the United States, many others are recent immigrants (see Chapters 1 and 2); yet the national data do not indicate these distinctions. Envi- ronmental exposures experienced in Asia, such as women's exposure to smoke from cooking fuels, may influence lung cancer occurrence among recent immi- grants (Co&as et al. 1994). From 1980 through 1995, age-adjusted death rate for malignant neoplasms of the respiratory system (primarily deaths from lung cancer) among Asian Table 3. Death rates for lung cancer among American Indians and Alaska Natives, by Indian Health Service (IHS) area, 1984-1988 Areas Men Women N Rate* N Rate* U.S., all ethnicities Nine IHS areas*+ All 12 IHS areas Aberdeen Alaska Albuquerque Bemidji Billings California+ Nashville Navajo Oklahoma+ Phoenix Portland+ Tucson 74.2 27.3 307 38.5$ 203 27.2 562 40.1t 296 21.4i 63 68.7 41 45.01 80 75.5 62 68.5$ 12 18.8$ 5 7.8$ 41 63.4$ 24 40.71 36 65.3 33 65.7i 33 33.2' 8 6.6$ 24 41.8t 15 25.1 25 11.4i 7 4.0$ 167 46.0i 55 14.0$ 20 17.2$ 13 11.5* 55 40.5f 30 23.4 6 25.9i 3 13.5i *Per 100,000, age-adjusted to the 1970 U.S. standard population. Rates based on a small number of deaths should be interpreted with caution. `The California, Oklahoma, and Portland IHS areas appear to have a problem with underreporting Indian ethnicity on death certificates; therefore, a separate total is presented for the nine other IHS areas, excluding these three areas. iDenotes a rate significantlv different from the rate for the overall U.S. population. Source: Valway 1992. During 1988-1992, the age-adjusted (to the 1970 U.S. standard population) incidence per 100,000 popu- lation of lung cancer for men was 89.0 for Hawaiians, 70.9 for Vietnamese, 53.2 for Koreans, 52.6 for Filipi- nos, 52.1 for Chinese, and 43.0 for Japanese. For com- parison purposes, the lung cancer incidence rates were 117.0 for African American men, 76.0 for white men, and 41.8 for Hispanic men. For women, the lung can- cer incidence rates were 43.1 for Hawaiians, 31.2 for Vietnamese, 25.3 for Chinese, 17.5 for Filipinos, 16.0 for Koreans, and 15.2 for Japanese. In comparison, the lung cancer incidence rates were 44.2 for African American women, 41.5 for white women, and 19.5 for Hispanic women. American and Pacific Islander men remained fairly Age-adjusted lung cancer death rates during constant; this death rate for Asian American and Pa- 1988-1992 were, per 100,000 men, 88.9 for Hawaiians, cific Islander women increased slightly between 1980 40.1 for Chinese, 32.4 for Japanese, and 29.8 for Filipi- and 1995 but was substantially lower than for men nos; mortality estimates were not available for Kore- (Table 1) (NCHS 1997). Trends should be interpreted ans and Vietnamese of either gender. In comparison, with caution because the large numbers of immigrants the lung cancer death rates were 105.6 for African from Asia and the Pacific Islands that came to the American men, 72.6 for white men, and 32.4 for His- United States during that time may have influenced panic men. For women, the lung cancer death rates both disease prevalence in and the age structure of this were 44.1 for Hawaiians, 18.5 for Chinese, 12.9 for Japa- group. During 1992-1994, the age-adjusted death rate nese, and 10.0 for Filipinos. In comparison, the lung for lung cancer was 27.9 per 100,000 for Asian Ameri- cancer death rates were 31.9 for white women, 31.5 can and Pacific Islander men and 11.4 per 100,000 for for African American women, and 10.8 for Hispanic women (Table 2). These rates were slightly higher than women (NC1 1996b). The lung cancer rates reflect gen- those for Hispanics and slightly lower than those for der differences in smoking rates among Asian Ameri- American Indians and Alaska Natives. In 1993, the can and Pacific Islander populations, as indicated by four leading causes of cancer death among Asian 1978-1995 data from the NHISs (see Chapter 2). Americans and Pacific Islanders were lung cancer (22.3 percent of all cancer deaths), cancer of the colon and rectum (10.4 percent), cancer of the liver and intrahe- patic bile duct (8.6 percent), and stomach cancer (7.7 percent) (Parker et al. 1997). Data on lung cancer for more specific subgroups have been published in several reports (Baquet et al. 1986; Ross et al. 1991; Zane et al. 1994; NC1 1996b). The most recent data are from NCI's SEER program and provide information for 1988-1992. This report includes incidence data from the nine areas included in the annual SEER reports (e.g., Kosary et al. 1995) and from Los Angeles, San Jose/Monterey, and the Alaska Area Native Health Service. Data on Hispan- ics are predominantly from Los Angeles, New Mexico, San Francisco, and San Jose/Monterey. Most Hispan- ics represented in SEER are Mexican Americans. Data on Asian Americans and Pacific Islanders are mainly from Los Angeles, Hawaii, San Francisco/Oakland, San Jose/Monterey, and Seattle/Puget Sound. Data on American Indians are from New Mexico; data from the Alaska Native Area Health Service provide infor- mation on Alaska Natives (NC1 1996b). Tohncco Use Among U.S. Racinl/Ethic Mirzority Groups Several studies have identified high rates of lung cancer among Native Hawaiians. Data on lung cancer among Pacific Islanders from the Hawaii Tumor Regis- try indicate that Native Hawaiians have the highest lung cancer incidence rates among the islands' other racial/ethnic groups, including Japanese, Filipinos, and Chinese (Kolonell980; Hinds et al. 1981). Using medi- cal records of lung cancer patients and data from a population-based survey, Hinds and colleagues (19811 assessed the risk of developing lung cancer associated with smoking among M'omen in Hawaii. The risk for developing lung cancer among women ~~110 had e\`er smoked compared with those ~`1~0 had never smoked w'as substantially greater among Nati\-e Harvaiian women (tenfold higher) than among Japanese women (fivefold higher) and Chinese women (tlvofold higher). In a comparison of the risks of smoking among Natilre Hawaiians, Filipinos, Japanese, and Chinese in HawFaii, Le Marchand and colleagues (1992) found that Native Hawaiian men had the highest risk and that lvhite and Filipino women had higher risks than Native Hawai- ian women. The pattern of variation of smoking's effect on lung cancer \vas statistically significant for men. These differences persisted after variables for beta-carotene and cholesterol intake were included in the statistical model. The observation that the risk of lung cancer related to smoking may vary among sub- groups requires further elucidation. In a cohort study of 7,961 Japanese American men who were living in Hawaii, the incidence of lung cancer was 11.4 times higher in current smokers than in persons ~`110 had never smoked; the risk for former smokers was 3.1 times higher than for never smokers (Chyou et al. 1993). Hispanics According to NCHS data from 1985 through 1995, the age-adjusted death rate for malignant neoplasms of the respiratory system (primarily deaths from lung cancer) among Hispanic men was about three times higher than that for Hispanic women (Table 1) (NCHS 1997). Trends should be interpreted with caution, be- cause only 17 states and the District of Columbia con- tributed death certificate data on Hispanics for 1985; by 1990, however, 47 states and the District of Colum- bia, covering 99.6 percent of the U.S. Hispanic popu- lation, contributed relevant data (Table 1) (NCHS 1997). From 1992 through 1994, the age-adjusted death rate for cancer of the trachea, bronchus, and lung (gener- ally referred to as lung cancer) was 23.1 per 100,000 for Hispanic men and 7.7 per 100,000 for Hispanic women (Table 2). Overall, lung cancer is the leading cause of cancer death among Hispanics. Among those who died of cancer in 1993, the four leading causes of death were lung cancer (17.9 percent), cancer of the colon and rectum (9.6 percent), cancer of the female breast (8.2 percent), and cancer of the liver and other biliary organs (6.0 percent) (Parker et al. 1997). Among Hispanic women, however, breast cancer mortality exceeds that of lung cancer (NC1 1996b). National mortality data for 1992-1994 (Table 4) also indicate that rates of lung cancer per 100,000 were higher among Cuban men (33.7) than among Mexican American (28.3) and Puerto Rican men (21.9). Among women, little variation is evident across His- panic subgroups (Table 4). An earlier nationwide analysis limited to foreign-born Cubans, Mexicans, and Puerto Ricans provided similar results for 1979-1981 (Rosenwaike 1987). Some regional data suggest that rates of lung cancer among Hispanics increased rapidly. For ex- ample, New Mexico mortality data for 1958-1982 indicate that lung cancer death rates increased for suc- cessive birth cohorts of Hispanics (Samet et al. 1988b). Between 1958-1962 and 19781982, lung cancer death rates per 100,000 increased from 10.1 to 28.8 among Hispanic men and from 4.8 to 11.2 among Hispanic women (Samet et al. 1988b). However, lung cancer death rates among Hispanics remained below those of the general U.S. population. Moreover, be- tween 1969-1971 and 1979-1981, lung cancer incidence rates doubled for persons with Spanish surnames (not necessarily all persons were Hispanic) residing in the Denver, Colorado, area (Savitz 1986). National and regional vital statistics have shown that patterns of lung cancer incidence differ among Hispanics and whites throughout the United States (NCHS 1994). Much of the information available on lung cancer incidence has relied on the SEER Program, which for many years included only one subgroup of Hispanics-those residing in New Mexico. Since the 195Os, descriptive studies of death have documented differing patterns of lung cancer among Hispanics and whites in the western and southwestern United States. In California, during the 1950s and 196Os, age-specific death rates from lung cancer among older Mexican-born women were two to three times the rates among California women of all ages (Buechley et al. 1957; Buell et al. 1968). Lung cancer death rates for women in Texas and New Mexico during the 1960s and 1970s showed a similar pattern of age-specific rates (Lee et al. 1976; Samet et al. 1980,1988b), although Hispanic women in the West and Southwest have had lower over- all lung cancer death rates than white women (Savitz 1986; Martin and Suarez 1987; Samet et al. 1988b; Bernstein and Ross 1991). Table 4. Age-adjusted death rates* for selected smoking-related causes of death among Mexican Americans, Puerto Rican Americans, and Cuban Americans, United States, 1992-1994 Disease category (ICD-9 code)+ Mexican Men Women Puerto Rican Men Women Cuban Men Women Cancer Lip, oral cavity, pharynx (140-149) Esophagus (150) Stomach (151) Pancreas (157) Larynx (161) Trachea, bronchus, lung (162) Cervix uteri (180) Bladder (188) Kidney, other, unspecified urinary organs (189) Cardiovascular diseases Coronary heart disease (410-414) Cerebrovascular disease (430338) 2.0 0.4 5.5 0.9 3.3 0.7 2.7 0.3 6.1 1.1 2.7 0.4 6.8 3.5 7.7 3.9 3.1 1.3 5.4 4.3 5.0 3.6 5.0 4.1 1.1 0.1 2.6 0.3 2.2 0.1 21.9 8.0 28.3 9.6 33.7 8.9 NA 3.7 NA 3.7 NA 1.6 1.4 0.5 2.1 1.0 3.5 0.5 3.7 1.6 1.9 1.0 2.7 1.0 82.3 44.2 25.5 18.9 118.6 67.3 95.2 42.4 27.3 16.5 17.1 11.5 Respiratory diseases Bronchitis, emphysema (491-492) Chronic airway obstruction, not elsewhere classified (496) 2.2 0.9 3.2 1.3 3.3 1.0 7.6 3.7 10.5 5.3 9.1 3.1 *Per 100,000, age-adjusted to the 1940 U.S. standard population. Death rates are not available from New Hampshire for 1992 and from Oklahoma for 1992-1994. Due to limitations in the data, the population estimates for Oklahoma and New, Hampshire were not subtracted from the denominator. Based on the 1990 Census, the number of persons of Hispanic origin from New, Hampshire and Oklahoma represented about 0.04 percent of the U.S. Hispanic population. +l~zfernnfio~~~/ Clnssificnfior~ of Disen.scs, Nirlfh R~~isicjr~, World Health Organization 1977. NA = data not available. Sources: National Center for Health Statistics, public use data tapes, 1992-1994; U.S. Bureau of the Census 1997. In 1982 and 1983, lung cancer rates among Hispanic men than among white men in New Mex- Hispanic men and women in Florida also were lower ico (Samet et al. 1980), Texas (Lee et al. 1976), Califor- than the rates among whites (Trapido et al. 1990a,b). nia (Menck et al. 1975; Bernstein and Ross 1991), More recent data (1981-1989) from Dade County, Connecticut (Polednak 19931, and Colorado (Savitz Florida, again show the incidence of lung cancer to be 1986). Mortality data indicate that Puerto Ricans lower among Hispanic men than among white men living on Long Island, New York, had slightly and lower among Hispanic women than white women lower death rates for lung cancer than Puerto Ricans (Trapido et al. 1994a,b). Similarly, Mexican and Puerto living elsewhere in the United States (except Puerto Rican immigrants in Illinois have had lower standard- Rico) (Polednak 1991). However, Puerto Rican men ized lung cancer death rates than whites (Mallin and and women residing on Long Island had lung cancer Anderson 1988). In addition, lung cancer incidence death rates that were three to four times the rates and death rates have been much lower among among Puerto Rico residents. These lower rates of lung cancer among Hispan- ics appear to reflect differences in smoking between Hispanics and whites. The results of a 1980-1982 case-control study of lung cancer cases among Hispan- ics and whites residing in New Mexico indicate that the risks (adjusted for gender and age) across catego- ries of smoking consumption among both groups were comparable (Table 5) (Humble et al. 1985). This find- ing suggests that the reduced rates of lung cancer deaths among Hispanics are attributable to their lower cigarette consumption (number of cigarettes smoked daily) and not to some other correlate of Hispanic race/ ethnicity. In a mortality study conducted in Texas be- tween 1970 and 1979 using age-standardized death rates, Holck and colleagues (1982) found that Mexi- can American women had stable lung cancer death rates (approximatelv 30 per lOO,OOO), whereas white Lvomen had increasing rates of death from lung cancer. The lower lung cancer rates for Mexican American women were consistent with their lower prevalence of smoking (18.5 percent of Mexican Ameri- can women vs. 31.6 percent of white women). The elevated rates of lung cancer death among older Hispanic women in the West and Southwest ha\re been attributed to a possible pattern of early initiation of smoking among women born in Mexico before 1900 as well as the custom of cooking indoors with an open fire (Buell et al. 1968; Lee et al. 1976). The findings of a 1980-1982 case-control study in Ne\v Mexico indicate that older Hispanic women smoked hand-rolled ciga- rettes, which may have contributed to the high lung cancer death rate among older Mexican American women (Humble et al. 1985). Table 5. Odds ratios for the risk of lung cancer, by gender, racejethnicity, and smoking status, case-control study, New Mexico,* 1980-1982 Men Smoking status Former smokers Current smokers ~20 cigarettes per day 220 cigarettes per day Hispanic White 8.0+ 7.2 (1.942.2$ (3.0-17.6) 11.6 9.2 (2.7-61.5) (3.3-25.8) 26.1 24.7 (5.6-146.6) (10.0-59.9) Women Hispanic White Former smokers Current smokers ~20 cigarettes per day ~20 cigarettes per day 6.3+ 6.5 (1.5-27.8) (2.8-15.4) 18.5 19.2 (4.9-72.4) (6.5-60.8) 36.9 16.0 (7.6-217.1) (6.7-36.3) "Mantel-Haenszel estimates of exposure odds ratios were calculated for two age strata: ~65 years of age and 265 years of age. Odds ratios are relative to persons who never smoked. +p