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Pnttcms of Tobacco Use  133


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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<ide1lce data for metropolitan areas have shown that
the African American-white gradient in lung cancer
occurrence among men was consistent with gradients
in socioeconomic indicators (Devesa and Diamond
1983; Baquet et al. 1991) and that the difference in lung
c`lncfr disappeared when the data were adjusted for
\,ocioeconomic status. The authors of one paper
tB,lquet et al. 1991) surmised that the differences in
+moking patterns associated with socioeconomic sta-
tLl> ,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,>ly<es of cigarette smoking prevalence in the 1900s
tcjr African Americans and whites of both genders
(`I'~>ll~~\~ 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 <O.Ol.

t95% Cornfield confidence limits; unless otherwise
indicated, p <O.OOOl.
Source: Adapted from Humble et al. 1985.

Other Cancers

  Cigarette smoking causes cancers of the lung,
larynx, mouth, esophagus, and bladder; is a contrib-
uting factor for cancers of the pancreas, kidney, and
cervix; and is associated with cancer of the stomach
(USDHHS 1989b, 1990). Cigarette smoking is also sus-
pected of contributing to colon cancer (Giovanucci et
al. 1994), liver cancer (Doll et al. 1994), and acute
myeloid leukemia (Siegel 1993). Little information is
available on cigarette smoking as a risk factor for these
cancers among members of racial/ethnic minority
groups. In the annual Cancer Statistics Review of the

SEER Program, cancer incidence and death rates are
reported for African Americans and whites (Kosary et
al. 1995). A special 1986 report provides more detailed
information on African Americans and other ethnic
groups for 1978-1981 (Baquet et al. 1986). A more re-
cent report provides detailed information on several
ethnic groups for 1988-1992 (NC1 1996b). Other
population-based cancer registries are also beginning
to contribute relevant information.

  Several recently published sources of information
on cancer among American Indians include an IHS


report, which describes regional differences in cancer
deaths among American Indians in the United States
for 1984-1988 and time trends for 1968-1987 (Valway
1992); two reports from the Alaska Area Native Health
Service (Lanier et al. 1993, 1996), which describe can-
cer incidence in the state's Eskimo, Aleut, and Indian

populations; and an NC1 monograph that documents
the status of the evidence on cancer and the need for
additional research regarding cancer among American
Indians and Alaska Natives (Burhansstipanov and
Dresser 1993).

Table 6.  Age-adjusted incidence and death rates* for selected smoking-related cancers, by race/ethnicity and
    gender, National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program,
      1988-1992

Primary cancer site       African
UCD-9 code)+          American

Alaska
Native

American
  Indian
(New Mexico)

Chinese

Filipino

All sites
Incidence rate,5 men
Incidence rate, women
Death rate,1 men
Death rate, women

Cervix uteri (180)
Incidence rate, women
Death rate, women

560,'        372         196         282        274
326        348         180         213         224
319         225         123         139         105
168         179         99          86         63

13.2        15.8
6.7           -**

9.9         7.3         9.6
-           2.6         2.4

Esophagus (150)
Incidence rate, men
Incidence rate, women
Death rate, men
Death rate, women

Kidney and renal pelvis
(189.0-189.1)
Incidence rate, men
Incidence rate, women
Death rate, men
Death rate, women

Larynx (161)
Incidence rate, men
Incidence rate, women
Death rate, men
Death rate, women

Lung and bronchus
(162.2-162.9)
Incidence rate, men
Incidence rate, women
Death rate, men
Death rate, women

15.0
4.4
14.8
3.7

5.3
-
4.2
-

2.9
2.2
-

-

-

-

-

12.8
6.0
5.1
2.2

15.6
-

4.6         5.8
2.3         2.8
1.3         1.9
0.9            -

-

-

12.7
2.5
5.6
0.9

2.8
-
0.9
-

2.4
-

-

-

-

117.0        81.1
44.2        50.6
105.6        69.4
31.5        45.3

52.1         52.6
25.3        17.5
40.1        29.8
18.5        10.0

*Rates per 100,000, age-adjusted to the 1970 U.S. standard population.
W.S. Department of Health and Human Services 1989a.
`Includes persons of other ethnic groups who designated themselves as of Hispanic origin.
$A11 incidence data are from five states: Connecticut, Hawaii, Iowa, New Mexico, and Utah; from six
metropolitan areas: Atlanta (including 10 rural counties), Detroit, Los Angeles, San Francisco/Oakland,
San Jose/Monterey, and Seattle/Puget Sound; and from the Alaska Area Native Health Service.

1.50 Chnyter 3


7obclcco Use Ammo U.S. RnciallEfhnic Minority Groups

   Death and incidence data both indicate marked   than whites for a number of smoking-related cancer sites,
heterogeneity of cancer occurrence among racial/   including the oral cavity and pharynx, esophagus, cer-
ethnic groups in the United States, and this heteroge-   vix uteri, larynx, stomach, pancreas, and lung (Table 6;
neity extends to the cancer sites associated with ciga-   Figure 4) (Kosary et al. 1995; NC1 1996b). When the ra-
rette smoking. For example, SEER data indicate that   tios of African American to white incidence and death
African Americans have higher incidence and death rates   rates exceed 1.0 in Figure 4, then African Americans

Hawaiian

Japanese

Korean

Vietnamese

White

Hispanic%

340         322         266
321         241         180
239         133        NA
168          88         NA

326        469        319
273         346         243
NA         213        129
NA         140         85

9.3
-

5.8         15.2
1.5       NA

43.0         8.7        16.2
NA          2.5         3.4

9.4
-

5.6

5.4
1.7
5.3
1.2

4.4
0.9
3.4
0.7

-

-
NA
NA

NA
NA

4.8
0.9

9.8
-

7.3
2.3
2.4
0.8

6.3
NA
NA

11.9
5.9
5.0
2.3

10.0
5.5
3.7
1.7

5.1
0.7
1.9
0.2

  -
NA
NA

2.5

7.5
1.5
2.3
0.5

-

  -
NA
NA

-

70.9        76.0        41.8
31.2        41.5        19.5
NA         72.6        32.4
NA          31.9        10.8

89.0        43.0        53.2
43.1         15.2        16.0
88.9        32.4        NA
44.1        12.9       NA

`Estimates for all cancer sites are rounded to the nearest integer.
TNational Center for Health Statistics, public use data tapes, 1988-1992, is the source for all death rates
in this table. Death rates are U.S. mortality rates.
**A dash means that the rate was not calculated for fewer than 25 cases.
NA = data not available.
Source: National Cancer Institute 1996b; National Center for Health Statistics, public use data tapes, 1988-1992.

Hmltlr Consequences 152


Table 6. Continued

                                      American
Primary cancer site        African      Alaska      Indian
(ZCD-9 code)+           American     Native    (New Mexico)    Chinese    Filipino

Oral cavity excluding
nasopharynx
(140.0-146.9; 148.0-149.9)
Incidence rate,+ men        20.4'           -**            -           5.3         5.4
Incidence rate, women       5.8            -                     2.3         5.3
Death rate, men           8.7            -                    1.6         1.2
Death rate, women         2.1            -             -           0.7         1.3

Pancreas (1.57)
Incidence rate, men        14.0            -                    8.0         6.5
Incidence rate, women      11.5            -                     4.9         6.0
Death rate,' men          14.4            -                     6.7         4.5
Death rate, women         10.4            -             -           5.1         3.5

Stomach (151)
Incidence rate, men        17.9        27.2                   15.7         8.5
Incidence rate, women       7.6            -             -          8.3         5.3
Death rate, men           13.6            -             -          10.5         3.6
Death rate, women         5.6            -             -           4.8         2.5

Urinary bladder (188)
Incidence rate, men         15.2            -             -          13.0         8.3
Incidence rate, women       5.8            -             -           3.7         2.1
Death rate, men           4.8            -             -           2.0          1.2
Death rate, women          2.4            -             -          1.0            -

*Rates per 100,000, age-adjusted to the 1970 U.S. standard population.
W.S. Department of Health and Human Services 1989a.
XIncludes persons of other ethnic groups who designated themselves as of Hispanic origin.
<All incidence data are from five states: Connecticut, Hawaii, Iowa, New Mexico, and Utah; from six
metropolitan areas: Atlanta (including 10 rural counties), Detroit, Los Angeles, San Francisco/Oakland,
San Jose/Monterey, and Seattle/Puget Sound; and from the Alaska Area Native Health Service.

experience excess morbidity and mortality from the can
cers shown. Also, SEER data for 1988-1992 show that
whites have higher rates of some cancers than Hispan-
ics, Asian Americans, Pacific Islanders, American In-
dians, and Alaska Natives (Table 6) (NC1 1996b). U.S.
mortality data for 1984-1988 show that American In-
dians have a lower mortality rate from lung cancer than
the general U.S. population but a higher mortality rate
from cervical cancer (Table 7) (Valway 19921.

Cervical Cancer

  In a case-control Los Angeles County study of
invasive cervical cancer that included 98 English-
speaking case-control pairs and 102 Spanish-speaking

pairs, Peters and colleagues (1986) found that the over-
all risk of such cancer was increased by cigarette smok-
ing. The cervical cancer risk related to smoking was
comparable in the two groups. In a more recent study
of the risk factors for cervical dysplasia among
Hispanic and white women in New Mexico (Becker et
al. 1994a,b), cigarette smoking was significantly asso-
ciated with high-grade cervical dysplasia among white
women but not among Hispanic women; however, this
difference in risk was not statistically significant. In
addition, in a recent pilot study of American Indian
women in the Albuquerque IHS area, Becker and
colleagues (1993) found that cigarette smoking was
associated with cervical dysplasia; however, the results
were not statistically significant.