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Explaining low Mortality Among US Immigrants Relative to Native-Born Americans: The Role of Smoking

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In many developed countries, immigrants live longer-that is, have lower death rates at most or all ages-than native-born residents. This article tests whether different levels of smoking-related mortality can explain part of the 'healthy immigrant effect' in the USA, as well as part of the related 'Hispanic paradox': the tendency for US Hispanics to outlive non-Hispanic Whites. With data from vital statistics and the national census, we calculate lung cancer death rates in 2000 for four US subpopulations: foreign-born, native-born, Hispanic and non-Hispanic White. We then use three different methods-the Peto-Lopez method, the Preston-Glei-Wilmoth method and a novel method developed in this article-to generate three alternative estimates of smoking-related mortality for each of the four subpopulations, extrapolating from lung cancer death rates. We then measure the contribution of smoking-related mortality to disparities in all-cause mortality. Taking estimates from any of the three methods, we find that smoking explains >50% of the difference in life expectancy at 50 years between foreign- and native-born men, and >70% of the difference between foreign- and native-born women; smoking explains >75% of the difference in life expectancy at 50 years between US Hispanic and non-Hispanic White men, and close to 75% of the Hispanic advantage among women. Low smoking-related mortality was the main reason for immigrants' and Hispanics' longevity advantage in the USA in 2000.
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OTHER ORIGINAL ARTICLES
Explaining low mortality among US immigrants
relative to native-born Americans: the role
of smoking
Laura Blue
1
* and Andrew Fenelon
2
1
Office of Population Research, Princeton University, Princeton, NJ, USA and
2
Department of Sociology and Population Studies
Center, University of Pennsylvania, Philadelphia, PA, USA
*Corresponding author. Office of Population Research, Wallace Hall (Floor 2), Princeton University, Princeton, NJ 08544, USA.
E-mail: lblue@princeton.edu
Accepted 11 January 2011
Background In many developed countries, immigrants live longer—that is, have
lower death rates at most or all ages—than native-born residents.
This article tests whether different levels of smoking-related mor-
tality can explain part of the ‘healthy immigrant effect’ in the USA,
as well as part of the related ‘Hispanic paradox’: the tendency for
US Hispanics to outlive non-Hispanic Whites.
Methods With data from vital statistics and the national census, we calculate
lung cancer death rates in 2000 for four US subpopulations:
foreign-born, native-born, Hispanic and non-Hispanic White. We
then use three different methods—the Peto–Lopez method, the
Preston–Glei–Wilmoth method and a novel method developed in
this article—to generate three alternative estimates of smoking-
related mortality for each of the four subpopulations, extrapolating
from lung cancer death rates. We then measure the contribution of
smoking-related mortality to disparities in all-cause mortality.
Results Taking estimates from any of the three methods, we find that
smoking explains 450% of the difference in life expectancy at
50 years between foreign- and native-born men, and 470% of the
difference between foreign- and native-born women; smoking ex-
plains 475% of the difference in life expectancy at 50 years between
US Hispanic and non-Hispanic White men, and close to 75% of the
Hispanic advantage among women.
Conclusions Low smoking-related mortality was the main reason for immi-
grants’ and Hispanics’ longevity advantage in the USA in 2000.
Keywords Health status disparities, minority health, smoking, lung neoplasms,
mortality, statistics as topic
Introduction
In many developed countries, including Australia,
1
Canada,
2
Germany
3
and the USA,
4
immigrants appear
to outlive native-born residents, with lower death
rates at most or all ages. Scholars have been puzzled
by this ‘healthy immigrant’ (or ‘healthy migrant’)
effect—sometimes also called the ‘immigrant para-
dox’—as it runs counter to an otherwise persistent
trend for richer and better-educated populations to
Published by Oxford University Press on behalf of the International Epidemiological Association
ßThe Author 2011; all rights reserved. Advance Access publication 15 February 2011
International Journal of Epidemiology 2011;40:786–793
doi:10.1093/ije/dyr011
786
live longer. In the USA, for example, immigrants are
not only less well educated, less wealthy and more
likely to live in poverty,
5
but also often have poorer
access to health care. For similar reasons, scholars
have been perplexed by the ‘Hispanic paradox’: a ten-
dency for US Hispanics to live longer
6
and healthier
lives than non-Hispanic Whites.
There are several hypotheses to explain immigrants’
life expectancy advantage. Kennedy et al.
7
found evi-
dence for migrant self-selection—that people who are
relatively healthy find it easier to settle in new coun-
tries. There is also some evidence for selection in
return migration—a so-called ‘salmon bias’ effect,
where unhealthy migrants are more likely than
healthy ones to return to their countries of origin,
8
although Turra and Elo
9
suggest this can explain
only some fraction of migrants’ and Hispanics’ lon-
gevity advantage in the USA. Finally, immigrants may
maintain healthier lifestyles in their host country
than native-born residents. A study of adolescent be-
haviour
10
shows that California minority immigrants,
for example, eat more fruit and vegetables and drink
less soda than the state’s non-Hispanic White adoles-
cent population. Foreign-born adults in the USA also
have lower rates of obesity than native-born
Americans.
11
We suggest that smoking habits may contribute to im-
migrants’ relative good health, at least in the USA.
Immigrants and Hispanics are less likely to be current
smokers
12,13
or former smokers
13
than native-born US
Whites. Although the differences in smoking prevalence
are only 2 percentage points among men and 6
among women, smoking-attributable mortality is af-
fected not only by current behaviour, but also by past
behaviour. People dying of smoking-related diseases
today—almost always people in middle age or older—
most likely began smoking as teenagers or young adults
in the 1950s through 1970s, a period of relatively heavy
tobacco use in the USA. Figures from the National
Center for Health Statistics (NCHS) put smoking preva-
lence in the mid-1960s at 51% among adult men and
33% among adult women.
14
Using individual-level data, Denney et al.
15
show
that Hispanics’ survival advantage is attenuated once
controls for smoking status are introduced. However,
such studies may still fail to capture the full impact of
smoking if—as reports from the National Health
Interview Survey suggest
13
—Hispanic smokers are
typically lighter smokers than other smokers are.
Indirect methods may yield more robust estimates of
smoking-attributable mortality.
Methods
We estimate the contribution of smoking-attributable
mortality to all-cause mortality disparities observed in
2000 between foreign-born US residents and native-
born Americans, and between US Hispanics and non-
Hispanic Whites.
We use three different methods to generate, for each
analysis, three alternative estimates of smoking-
attributable mortality. All three methods use the
death rate from lung cancer as a marker of accumu-
lated smoking exposure within a population. This ap-
proach is supported by a large research literature that
shows smoking to be the main source of variation in
lung cancer mortality among populations.
16–18
Our
three methods are the Peto–Lopez method,
19,20
which extrapolates smoking-related mortality from
lung cancer mortality based on risks observed
among smokers in the Cancer Prevention Study II;
the newer Preston–Glei–Wilmoth (PGW) method,
21
which instead extrapolates smoking-related deaths
from correlations between lung cancer mortality and
mortality from other causes across 20 high-income
countries; and a novel indirect estimation technique,
outlined below. While all three methods make broadly
similar assumptions, they allow assumptions to be
relaxed in different ways.
Calculation of lung cancer mortality
For all three methods, we first calculated all-cause
mortality for the year 2000, tabulating age-specific
death rates by sex for four subpopulations: foreign-
born, native-born, Hispanic and non-Hispanic White
(Figure 1). We took rate numerators (deaths) from
the Multiple Cause-of-Death Public-Use Microdata
files, available from NCHS. These data include dece-
dents’ race, ethnicity and place of birth, as recorded
on each person’s death certificate. From a total of
2 407 193 deaths in 2000, we dropped 363 entries
without a recorded age and 14 378 with missing
place of birth. We followed the death certificate clas-
sification of ‘Hispanic’ and ‘non-Hispanic White’. We
considered anyone born outside the 50 US states and
the District of Columbia to be ‘foreign-born’, and
anyone born inside to be ‘native-born’. We took our
rate denominators (population counts) from the US
2000 Census 5% Public Use Microdata Sample Files.
These data, too, provide individual-level records on
race, ethnicity and place of birth. Using these same
data sources, we then calculated age- and sex-specific
death rates in 2000 for lung cancer only, using as our
numerator the number of deaths indicated on death
certificates as attributable to lung cancer
[International Classification of Diseases (ICD)-10
codes C33–C34].
A new method to estimate
smoking-attributable mortality
We have developed a new method to estimate smok-
ing-attributable mortality. Our method builds on the
familiar assumption that lung cancer mortality is a
reliable marker of smoking exposure in a population.
Not all lung cancers are caused by smoking, and lung
cancer is not the only deadly smoking-related condi-
tion. However, if we know both the proportion of
lung cancers caused by smoking (P) and the
ROLE OF SMOKING IN LOW MORTALITY AMONG US IMMIGRANTS 787
proportion of smoking-related mortality that is lung
cancer mortality (Q), we can estimate total smoking
deaths (D
S
) as follows:
DS¼PDL
Q
where D
L
is the number of lung cancer deaths.
A great deal of epidemiological work has focused on
the two proportions that we call here Pand Q.Pis
simply the attributable risk, the proportion of lung
cancer mortality that would not have occurred in
the absence of smoking:
P¼ðMLM
LÞ
ML
where M
L
is the observed population lung cancer
death rate, and M
Lis the lung cancer death rate
among members of that population who have never
smoked. It can be difficult to get precise M
Lvalues by
age and sex, since lung cancer deaths are rare among
never-smokers. However, Michael Thun et al.
22
have
recently produced such estimates, pooling together
rates from both US Cancer Prevention Studies, the
Nurses’ Health Study, the Women’s Health Study
and other major US and non-US trials and cohort
studies. We use the pooled estimates among never-
smoker Whites (both in the USA and abroad) as
our baseline risk for lung cancer mortality in the
absence of smoking. We then calculate Pby age and
sex for each subpopulation (see Supplementary
Appendix A for values, available as supplementary
data at IJE online).
We calculate Qfrom Centers for Disease Control and
Prevention (CDC) tabulations of smoking-related
mortality from 1997 to 2001.
23
During those years,
the CDC estimates that lung cancer caused 32% of
all smoking-attributable deaths among men and
29% among women, with the bulk of deaths due to
other conditions, including heart disease, chronic ob-
structive pulmonary disease and cancer of other
organs. In our calculations, therefore, we take Qas
0.32 for men and 0.29 for women. For simplicity,
we assume these values do not vary by age.
Sensitivity analyses
The Peto–Lopez and PGW methods assume that
excess lung cancer deaths and other smoking-
attributable deaths are related in the same way in
all populations. Our new method allows this assump-
tion to be relaxed. To test robustness, we use the new
method to calculate six different scenarios in addition
to our principal estimates.
Low estimate: we allow Pand Qto vary by subpo-
pulation. Pis calculated as in the principal analysis.
Among native-born Americans and non-Hispanic
Whites Q¼0.29 for females and Q¼0.32 for
males, as observed in the population at large.
Among immigrants and Hispanics, however,
Q¼0.24 for females and Q¼0.27 for males—arbi-
trarily set values that allow immigrants and
Hispanics to be unusually susceptible to non-lung
cancer smoking deaths.
High estimate: we allow Pand Qto vary by sub-
population. Pis calculated for native-born
Americans and non-Hispanic Whites as in the prin-
cipal analysis; for immigrants and Hispanics, it
is calculated from the never-smoker lung cancer
death rates among Asians compiled by Thun et al.
22
Among native-born Americans and non-Hispanic
Whites, Q¼0.29 for females and Q¼0.32 for males
as observed in the population at large. Among immi-
grants and Hispanics, Q¼0.34 for females and
Q¼0.37 for males—arbitrarily set values that allow
immigrants and Hispanics to be unusually resistant
to smoking-related deaths from causes other than
lung cancer.
Salmon bias correction: Pand Qare the same as
those from ‘low estimate’. We account here for the
possibility that observed deaths among immigrants
or Hispanics are only some fraction of true deaths,
as sick immigrants may leave the country to die.
0.001
0.01
0.1
1
50 55 60 65 70 75 80 85+
Females: native vs foreign born
Native Foreign
0.001
0.01
0.1
1
50 55 60 65 70 75 80 85+
Males: native vs foreign born
Native Foreign
Age
Death rate
Age
Death rate
Figure 1 US death rates (log scale) in 2000
788 INTERNATIONAL JOURNAL OF EPIDEMIOLOGY
Data from the Surveillance, Epidemiology and End
Results (SEER) Program
24
show that the ratio of
lung cancer mortality to lung cancer incidence is
higher for non-Hispanics (0.90 for men; 0.76 for
women) than for Hispanics (0.79 for men; 0.57
for women). This could be a sign of Hispanics’ se-
lective migration, or it could be that Hispanics have
lower case severity (perhaps because they smoke
less). Here, we assume the former, and inflate lung
cancer death rates for immigrants and Hispanics
by the full difference in mortality-to-incidence, multi-
plying by 1.14 for men and by 1.34 for women. [Data
on mortality-to-incidence exist only by ethnicity,
and not by place of birth. The mortality-to-incidence
ratio is 14% higher for non-Hispanic men than
Hispanic men (0.90/0.79 ¼1.14) and 34% higher for
non-Hispanic women relative to Hispanic women
(0.76/0.57 ¼1.34).]
½ Salmon bias correction: Pand Qare those from
‘low estimate’. Lung cancer death rates among im-
migrants and Hispanics are inflated by one-half of
the difference in SEER mortality-to-incidence ratios
observed between Hispanics and non-Hispanic
Whites. For foreign-born and Hispanic women,
lung cancer death rates are inflated by multiplying
by 0.5*(0.76/0.57 1) þ1¼1.16; for men, by
0.5*(0.90/0.79 1) þ1¼1.07.
Age-varying Q: we allow the proportion of smoking-
attributable deaths caused by lung cancer to vary by
age. We use the PGW method
21
and national data
for the USA in 2000 (described above) to calculate
new estimates of Q,bysex,foreach5-yearage
group.
Strong adjustment for possible confounding: taking
Qfrom the CDC assumes that all estimated excess
deaths among smokers are directly caused by smoking.
Here, we assume only half of smokers’ excess non-lung
cancer deaths are smoking-attributable. That is,
Q¼0.29/(0.29 þ[1 0.29]*0.5) ¼0.45 for women
and Q¼0.32/(0.32 þ[1 0.32]*0.5) ¼0.48 for men.
Results
In 2000, native-born Americans had substantially
higher lung cancer death rates than US immigrants,
and non-Hispanic Whites had substantially higher
rates than US Hispanics (Figure 2). Using three alter-
native methods, we estimate, as a result, that total
smoking-related mortality was also higher among
native-born Americans and non-Hispanic Whites
than among US immigrants and Hispanics. For each
method, we present detailed mortality estimates by
age and sex in Supplementary Appendix B (available
as supplementary data at IJE online).
0.0001
0.001
0.01
0.1
1
50 55 60 65 70 75 80 85+
Females: native vs foreign born
Native Foreign
0.0001
0.001
0.01
0.1
1
50 55 60 65 70 75 80 85+
Males: native vs foreign born
Native Foreign
0.0001
0.001
0.01
0.1
1
50 55 60 65 70 75 80 85+
Females: non-Hispanic vs Hispanic
Non-Hispanic White Hispanic
0.0001
0.001
0.01
0.1
1
50 55 60 65 70 75 80 85+
Males: non-Hispanic vs Hispanic
Non-Hispanic White Hispanic
Age
Lung cancer death rate
Age
Lung cancer death rate
Age
Lung cancer death rate
Age
Lung cancer death rate
Figure 2 US lung cancer death rates (log scale) in 2000
ROLE OF SMOKING IN LOW MORTALITY AMONG US IMMIGRANTS 789
We use Arriaga’s method
25
to decompose differences
in life expectancy at age 50 years into two compo-
nents: a component due to smoking and a component
due to other factors. Taking estimates from any of the
three methods, we find that smoking accounts for at
least 50% of migrants’ advantage in life expectancy at
50 years among men and at least 70% among women.
Smoking explains 475% of the difference in life ex-
pectancy at 50 years between US Hispanic and
non-Hispanic-White men, and close to 75% of this
difference among women (Figure 3).
Table 1 shows sensitivity-analysis results. In most of
the scenarios, smoking still accounts for 450% of the
differences in life expectancy at 50 years. In one in-
stance, smoking is estimated to explain 4100%; this
means that, in the absence of smoking, male life ex-
pectancy would be higher among non-Hispanic
Whites than among Hispanics.
Discussion
We find that low mortality from smoking is the main
reason for immigrants’ and Hispanics’ longevity ad-
vantage in the USA in 2000. While previous studies
have documented lower smoking prevalence among
US immigrants compared with native-born
Americans, and among Hispanics compared with
non-Hispanic Whites, to our knowledge none of
0
0.5
1
1.5
2
2.5
3
PL PGW BF PL PGW BF
Foreign born–native born
Other Factors
Smoking
Males
2.74 years
78.0% 72.2% 71.0% 66.8% 53.6% 58.3%
Females
2.09 years
0
0.5
1
1.5
2
2.5
3
PL PGW BF PL PGW BF
Hispanic–non-Hispanic White
Other Factors
Smoking
Males
2.11 years
76.2%74.8%75.3%77.7% 87.2%88.2%
Females
2.82 years
Life expectancy disparity (years)
Life expectancy disparity (years)
Figure 3 Differences in life expectancy at age 50 years and proportion explained by smoking, by nativity and ethnicity.
PL ¼Peto–Lopez method; PGW ¼Preston–Glei–Wilmoth method; BF ¼Blue–Fenelon method, developed in this article
790 INTERNATIONAL JOURNAL OF EPIDEMIOLOGY
these earlier studies calculates the contribution of
smoking to US mortality disparities.
Like other demographers and epidemiologists,
19–21,26
we believe lung cancer mortality is the most reliable
marker of a population’s smoking behaviour.
Mortality data are available by age and sex in many
developed countries, whereas detailed data on smok-
ing prevalence, duration and intensity generally are
not. To date, studies using indirect methods have typ-
ically found that smoking explains a greater propor-
tion of longevity differences than studies using direct
methods. For example, Jha et al.
27
(using the Peto–
Lopez method) found that smoking explains more
than half of the social gradient in mortality in
England and Wales, whereas English longitudinal stu-
dies generate estimates closer to one quarter.
28,29
Crude survey measurement of smoking habits may
explain part of the discrepancy. Surveys can suffer
from inaccurate self-reports, from non-response rates
that leave the sample of respondents unrepresentative
of the population at large, and—where participants
are followed over time—by unrecorded changes in
smoking behaviour. It is also difficult to measure
smoking intensity with precision; survey respondents
are usually asked to categorize their consumption into
large bins, such as ‘more than 20 cigarettes per day’
or ‘former smoker’.
In this article, we develop a new method to estimate
smoking-attributable deaths. Our technique is similar
to the widely accepted Peto–Lopez method, although
it is somewhat simpler; it ignores age variation in the
cause-of-death distribution. Our main advantage,
however, is the possibility of straightforward sensitiv-
ity checks. We can relax assumptions about Pand Q,
whereas the Peto–Lopez and PGW methods both
assume that never-smoker lung cancer risks will not
vary across populations (as they may with differences
in genetic susceptibility or in exposure to carcinogens
like asbestos or smoke from cooking fires). In prac-
tice, our new estimates of smoking-related mortality
appear quite similar to those generated using existing
methods.
We consider there to be two main sources of uncer-
tainty in our results. First, all three methods used in
this article assume that death certificates (and thus
the NCHS Multiple Cause-of-Death data) contain
complete and correct information on decedents’ birth-
place, race, ethnicity and cause of death. As noted
above, very few death records (<1%) are missing
entries for these variables. Our assumption is none-
theless complicated by the fact that race and Hispanic
status are identified differently in the Census (where
they are given by self-report) than they are in death
data (where reports are made by a third party).
However, although race and ethnicity misclassifi-
cation on death certificates may be more common
among immigrants and Hispanics than among
native-born non-Hispanics,
30
Arias et al.
31
show that
the magnitude of this bias is probably not great.
Furthermore, we see no obvious reason that these
classification errors should also vary systematically
and greatly by lung cancer as a cause of death. As a
result, errors in birthplace and ethnicity recorded on
death certificates may indeed cause us to overestimate
both the immigrant paradox and the Hispanic para-
dox, but, crucially, they should not greatly bias our
estimates of the proportion of these disparities that
are caused by smoking—provided that the direction
of the disparities is correct. We are confident that it
is. Cohort study results,
32
death data from Social
Security
9
and Medicare,
30
and new US life tables by
Hispanic origin
6
are unlikely to suffer the same mis-
classification errors. All show a clear Hispanic or im-
migrant advantage.
Secondly, for the new estimation technique, there is
some uncertainty in estimates of the key inputs, P
and Q. For simplicity, to calculate P, we have assumed
all US subpopulations would have identical lung
cancer death rates in the absence of smoking. We
chose to approximate this rate with the never-smoker
lung cancer death rates of Whites, compiled by Thun
et al.
22
Whites have the lowest rates of any of the race
in these authors’ global review. Using White rates
therefore generates the most conservative estimates
of the proportions of the immigrant paradox and
the Hispanic paradox that are due to smoking. If we
assumed instead that immigrants had the baseline
lung cancer risk of either Blacks or Asians in Thun
Table 1 Sensitivity analysis (from the new method to estimate smoking-attributable mortality): proportion of the differ-
ence in life expectancy at 50 years explained by smoking
Scenario
Foreign–native Hispanic–non-Hispanic White
Females (%) Males (%) Females (%) Males (%)
Principal estimate 71.02 58.27 75.33 88.17
Low estimate (Pand Qvary by subpopulation) 61.75 47.77 70.75 75.71
High estimate (Pand Qvary by subpopulation) 84.90 79.02 84.58 116.56
Low estimate with strong salmon-bias correction 43.84 38.42 61.89 64.61
Low estimate with ½ salmon-bias correction 52.79 43.10 66.32 70.16
Age-varying Q(with Qfrom PGW) 66.12 46.77 74.98 73.55
Strong adjustment for possible confounders 45.77 38.84 48.55 58.78
ROLE OF SMOKING IN LOW MORTALITY AMONG US IMMIGRANTS 791
et al.’s
22
analysis (as we do in the ‘high estimate’ of
the sensitivity analysis), we would estimate that
smoking explains a larger proportion still.
For our estimates of Q, the proportion of smoking-
related deaths that are lung cancer deaths, we import
figures from the CDC. Although we believe these fig-
ures are among the best available, they are based on
relative risks observed in cohort studies of smoking.
Past cohorts were rarely representative of the US
population, and it remains almost impossible to con-
trol fully for confounders that correlate smoking with
diseases not actually caused by smoking.
33
Furthermore, we cannot be certain that the cause-
of-death distribution of smoking deaths is constant
across subpopulations in which smoking-related mor-
tality has not been studied, and calculations using the
PGW method suggest this distribution does vary by
age, violating the assumption of age-invariant Q.We
consider several possible sources of error in our sen-
sitivity analysis. Ultimately, however, the input fig-
ures in these alternative scenarios are to some
degree arbitrary.
As it is unclear which assumptions about smoking-
related mortality may be most accurate, in this article
we have estimated the contribution of smoking to
mortality disparities using three different methods.
In addition, we have conducted sensitivity analysis
for six alternative scenarios, relaxing assumptions
about never-smoker lung cancer mortality, the
cause-of-death distribution of smoking-attributable
deaths, possible confounding and salmon bias. Many
of these scenarios are no doubt highly implausible.
Nevertheless, our estimates of the contribution
of smoking to mortality disparities are very similar
across all three methods, and are only moderately
sensitive to the assumptions changed in the sensitiv-
ity analysis. As a result, though one may doubt the
precision of figures we use to estimate smoking-
related mortality, we remain quite confident in our
conclusion: smoking is likely the major cause of
America’s immigrant paradox and the related
Hispanic paradox.
Supplementary Data
Supplementary data are available at IJE online.
Funding
This work was supported by the National Institutes of
Health (5T32 HD 007163 and 5T32 HD 007242–28).
Acknowledgements
We thank Samuel H. Preston and two anonymous
referees for their comments and guidance.
Conflict of interest: None declared.
KEY MESSAGES
In the USA, foreign-born residents have higher life expectancy than native-born Americans, and
Hispanics have higher life expectancy than non-Hispanic Whites, despite socioeconomic disadvan-
tages among the long-lived populations.
We hypothesize that smoking may account for some of these observed life expectancy differences by
nativity and ethnicity.
We use three different indirect methods—the Peto–Lopez method, the Preston–Glei–Wilmoth method
and a novel method outlined in this article—to estimate smoking-related mortality in 2000 for four
US subpopulations: foreign-born, native-born, Hispanic and non-Hispanic White.
Using any of the three indirect estimation techniques, we find that smoking explains more than half
of the difference in life expectancy at 50 years between foreign-born US residents and native-born
Americans, and close to three-quarters of the difference in life expectancy between US Hispanics and
non-Hispanic Whites.
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ROLE OF SMOKING IN LOW MORTALITY AMONG US IMMIGRANTS 793
... The findings on health outcomes other than mortality are more mixed, especially among older foreign-born individuals. For example, in the U.S., older immigrants report worse self-rated health [27,28] and have higher rates of disability than their native-born counterparts [29] but have lower rates of obesity, smoking, and alcohol consumption (e.g., [25,30]). The inconsistent results could be due to an imperfect relationship between mortality and morbidity and/or additional methodological challenges in measuring health, such as reporting biases and changes in health over the life course. ...
... Smoking is one of the most important health risk behaviors with well-documented genetic roots [39,40,53]. Research specifically points to smoking as one of the strongest predictors of mortality, and a possible explanation of the immigrant health advantage in mortality [9,30,32,33]. Immigrants are less likely to smoke than U.S.-born individuals or non-immigrants in their home countries [9,26,30,31]. However, the immigrant advantage is typically larger in comparison to non-migrants in their home countries, which is not surprising given that the smoking rates are higher in many immigrant origin countries than in the U.S., especially among males [31,55]. ...
... Research specifically points to smoking as one of the strongest predictors of mortality, and a possible explanation of the immigrant health advantage in mortality [9,30,32,33]. Immigrants are less likely to smoke than U.S.-born individuals or non-immigrants in their home countries [9,26,30,31]. However, the immigrant advantage is typically larger in comparison to non-migrants in their home countries, which is not surprising given that the smoking rates are higher in many immigrant origin countries than in the U.S., especially among males [31,55]. ...
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This study uses data from the 2006–2012 Health and Retirement Study (HRS) genetic sample (N = 11,667) to explore the “immigrant health paradox” from a novel perspective by examining the nativity differences in genetic predisposition to health-related outcomes. Polygenic indices (PGIs) were used to evaluate whether older non-Hispanic white foreign-born individuals have genotypes that predispose them to better health profiles compared to their U.S.-born counterparts. The results show an immigrant advantage with respect to genetic predisposition to cognitive function, BMI, and smoking frequency. There are no significant differences in genetic predisposition to height, smoking initiation, and depression. Including respective PGIs in multinomial regression models partially explains an immigrant advantage with respect to cognitive function and obesity. The findings are consistent with the “healthy immigrant effect” or selective migration of individuals with a favorable genetic predisposition to health as one of the explanations of the immigrant health paradox.
... Previous studies have documented lower mortality among foreign-born US residents than among their US-born counterparts (Blue and Fenelon 2011;Hendi and Ho 2021;Mehta et al. 2016;Singh and Miller 2004). Prior to the pandemic, smoking-related causes, cardiovascular diseases, and external causes contributed to the foreign-born mortality advantage (Fenelon 2013;Lariscy, Hummer, and Hayward 2014;Singh and Siahpush 2002). ...
... Yet the evidence remains inconclusive as to whether these preexisting conditions are systematically higher among the foreign born than among the US born. Foreign-born adults have lower prevalence of smoking (Blue and Fenelon 2011;Bosdriesz et al. 2013;Fenelon 2013) and obesity (Barrington et al. 2010;Mehta et al. 2015), though there is variability in the prevalence of diabetes and hypertension by race, Hispanic origin, and nativity (Choi, Narayan, and Patel 2022;Commodore-Mensah et al. 2018;Fang, Ayala, and Loustalot 2012;Mozaffarian et al. 2016;Zhang, Hayward, and Lu 2012). Nonetheless, it is unlikely that differences in comorbidities would account for the greater impact of the pandemic on the foreign born. ...
... Over this time period, Hispanic people consistently smoked at much lower rates than non-Hispanic White and African American people [44]. Blue and Fenelon concluded that low smoking-related deaths were the primary reason for the Hispanic population's longevity advantage over the non-Hispanic White population [45]. Besides lower smoking rates, a recently published study also found that American Latinos adhered to more heart-healthy diets [46]. ...
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Background After age 85, the U.S. non‐Hispanic Black population mortality rate becomes less than that of the White population (called the Black–White mortality crossover). It is not known how this survival advantage compares to Asian and Hispanic groups, and whether differences persist to age 100+ years. Methods The U.S. period life table data were extracted to obtain life expectancy at birth and at ages 70, 85, and 100 years according to year, sex, and race and ethnicity. Age‐specific death rates and adult modal age at death were calculated. We computed period probabilities of survival to age 100, from ages 70, 80, and 90. Pseudo‐birth cohort calculations were undertaken to enable comparison with period‐based results. Results In 2019, the Black–White mortality crossover occurred at 86–88 years and persisted at ages 100 and 100+. Life expectancies at age 100 for non‐Hispanic Black, Hispanic, and Asian populations were similar and were significantly greater than the non‐Hispanic White population. From 2006 to 2019, the probability of survival from 70 and 80 years to age 100 was highest for the Hispanic population, followed by non‐Hispanic Black and then non‐Hispanic White populations. Probability of survival from age 90 to 100 years was similar for all but the non‐Hispanic White population, which had a comparatively lower probability of survival. When Asian population data became available in 2019, this population had the highest probability of survival to age 100, starting from ages 70, 80, and 90 years. Pseudo‐cohort results displayed patterns consistent with those observed over calendar years. Conclusions Race‐ and ethnicity‐based variation in mortality between ages 85 and 100+ years suggests differences in environmental and possibly genetic influences upon risk for exceptional longevity.
... Similarly, studies focusing on other racial-ethnic groups, such as Asians and Blacks, have also revealed significant intragroup heterogeneity, further emphasizing the need for disaggregated data in health disparities research [43,48,49]. This heterogeneity among racial-ethnic subpopulations has been studied among other immigrant racial-ethnic groups including Asians and Blacks and has been coined the "healthy immigrant paradox" in past studies [50][51][52][53][54]. Therefore, exploring inter-and intra-group differences (i.e. ...
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Previous studies have identified racial-ethnic disparities in modifiable risk factors for cancers. However, the impact of US nativity on these risks is understudied. Hence, we assessed the association between US nativity and length of time in the US on modifiable cancer risk factors. Utilizing the 2010 and 2015 National Health Interview Survey datasets, we analyzed 8,861 US-born and non-US-born adults. Key variables included age, sex, race-ethnicity, education, income, diet, body mass index, physical activity, alcohol consumption, and smoking. Statistical methods included descriptive statistics and regression. Most respondents were US-born (n = 7,370), followed by long-term (≥15 years, n = 928), and recent (<15 years, n = 563) immigrants. Moderate-to-vigorous physical activity was higher among US-born individuals (342.45 minutes/week), compared to recent (249.74 minutes/week) and long-term immigrants (255.19 minutes/week). Recent immigrants consumed more fruits (1.37 cups/day) and long-term immigrants more vegetables (1.78 cups/day) than US-born individuals. Multivariate analyses found recent immigrants had lower odds of consuming alcohol (AOR: 0.33, 95% CI: 0.21–0.50) and smoking (AOR: 0.30, 95% CI: 0.19–0.46), and higher odds of meeting fruit consumption guidelines (AOR: 2.80, 95% CI: 1.76–4.45) compared to US-born individuals. Long-term immigrants had lower odds of alcohol consumption (AOR: 0.56, 95% CI: 0.37–0.84) and smoking (AOR: 0.42, 95% CI: 0.30–0.59), and higher odds for meeting fruit (AOR: 1.87, 95% CI: 1.22–2.86) and fiber (AOR: 2.03, 95% CI: 1.02–4.05) consumption guidelines. Our findings illustrate the importance of considering the impact nativity and length of US residency has on health. Our findings underscore the need for culturally tailored public health strategies.
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PURPOSE Hispanic and Latinx people in the United States are the fastest-growing ethnic group. However, previous studies in non–small-cell lung cancer (NSCLC) often analyze these diverse communities in aggregate. We aimed to identify differences in NSCLC stage at diagnosis in the US population, focusing on disaggregated Hispanic/Latinx individuals. METHODS Data from the National Cancer Database from 2004 to 2018 identified patients with primary NSCLC. Individuals were disaggregated by racial and ethnic subgroup and Hispanic country of origin. Ordinal logistic regression adjusting for age, facility type, income, educational attainment, comorbidity index, insurance, and year of diagnosis was used to create adjusted odds ratios (aORs), with higher odds representing diagnosis at later-stage NSCLC. RESULTS Of 1,565,159 patients with NSCLC, 46,616 were Hispanic/Latinx (3.0%). When analyzed in the setting of race and ethnicity, Hispanic patients were more likely to be diagnosed with metastatic disease compared with non-Hispanic White (NHW) patients: 47.0% for Hispanic Black, 46.0% Hispanic White, and 44.3% of Hispanic other patients versus 39.1% of non-Hispanic White patients ( P < .001 for all). By country of origin, 51.4% of Mexican, 41.7% of Puerto Rican, 44.6% of Cuban, 50.8% of South or Central American, 48.4% of Dominican, and 45.6% of other Hispanic patients were diagnosed with metastatic disease, compared with 39.1% of NHWs. Conversely, 20.2% of Mexican, 26.9% of Puerto Rican, 24.2% of Cuban, 22.5% of South or Central American, 23.7% of Dominican, and 24.5% of other Hispanic patients were diagnosed with stage I disease, compared with 30.0% of NHWs. All Hispanic groups were more likely to present with later-stage NSCLC than NHW patients (greatest odds for Mexican patients, aOR, 1.44; P < .001). CONCLUSION Hispanic/Latinx patients with non–small-cell lung cancer were more likely to be diagnosed with advanced disease compared with NHWs. Disparities persisted upon disaggregation by both race and country of origin, with over half of Mexican patients with metastatic disease at diagnosis. Disparities among Hispanic/Latinx groups by race and by country of origin highlight the shortcomings of treating these groups as a monolith and underscore the need for disaggregated research and targeted interventions.
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This report presents complete period life tables by Hispanic origin, race for the non-Hispanic white and non-Hispanic black populations, and sex for the United States based on age-specific death rates in 2006. The methods used to estimate the probability of death for ages 0-80 for the Hispanic population and 0-65 for the non-Hispanic white and non-Hispanic black populations are the same as those used in annual U.S. life tables since 1997, with an important modification. Age-specific death rates are first corrected for racial and ethnic misclassification on U.S. death certificates. To address the effects of age misstatement at the oldest ages, the methodology used to estimate mortality for ages 66 and over for the non-Hispanic white and non-Hispanic black populations is the same as that used to estimate the annual life tables since 2005. For the Hispanic population, the probability of death for ages over 80 is estimated as a function of non-Hispanic white mortality with the use of the Brass relational logit model. Life expectancy at birth for the total population in 2006 was 77.7 years; 80.6 years for the Hispanic population, 78.1 years for the non-Hispanic white population, and 72.9 years for the non-Hispanic black population. The Hispanic population has a life expectancy advantage at birth of 2.5 years over the non-Hispanic white population and 7.7 years over the non-Hispanic black population. Although seemingly paradoxical, these results are consistent with the findings of numerous studies which show a Hispanic mortality advantage despite this population's lower socioeconomic status. Nonetheless, the procedures used in this report to correct for racial and ethnic misclassification and age misstatement are not error free and therefore some of the observed advantage may still be a function of data artifact. This report does not address other factors that may explain the Hispanic mortality advantage.
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We tested the data artifact hypothesis regarding the Hispanic mortality advantage by investigating whether and to what degree this advantage is explained by Hispanic origin misclassification on US death certificates. We used the National Longitudinal Mortality Study, which links Current Population Survey records to death certificates for 1979 through 1998, to estimate the sensitivity, specificity, and net ascertainment of Hispanic ethnicity on death certificates compared with survey classifications. Using national vital statistics mortality data, we estimated Hispanic age-specific and age-adjusted death rates, which were uncorrected and corrected for death certificate misclassification, and produced death rate ratios comparing the Hispanic with the non-Hispanic White population. Hispanic origin reporting on death certificates in the United States is reasonably good. The net ascertainment of Hispanic origin is just 5% higher on survey records than on death certificates. Corrected age-adjusted death rates for Hispanics are lower than those for the non-Hispanic White population by close to 20%. The Hispanic mortality paradox is not explained by an incongruence between ethnic classification in vital registration and population data systems.
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Objective. —To compare all-cause and cause-specific mortality rates between Hispanic and non-Hispanic groups and estimate the effect of family income, place of birth, and place of residence on these rates.Design. —Cohort study using national survey data matched to the National Death Index, with a mortality follow-up period of 9 years.Setting. —The noninstitutionalized population of the United States.Participants. —Approximately 700000 respondents (aged 25 years or older), including 40 000 Hispanics, to national surveys conducted by the US Bureau of the Census (Current Population Surveys).Outcome Measures. —All causes and underlying cause of death, coded from the death certificate, occurring between 1979 and 1987.Results. —Adjusting for age, Hispanics were shown to have lower mortality from all causes compared with non-Hispanics (standardized rate ratio [SRR], 0.74 for men, 0.82 for women), lower mortality from cancer (SRR, 0.69 for men, 0.61 for women), lower mortality from cardiovascular disease (SRR, 0.65 for men, 0.80 for women), higher mortality from diabetes (SRR, 1.86 for men, 2.38 for women), and higher mortality from homicide (SRR, 3.60 for men). After adjusting for differences in annual family income, the relative mortality ratios were even lower for Hispanics than non-Hispanics.Conclusion. —These data describe, in a large national cohort study, a lower mortality in Hispanics than in non-Hispanics. This mortality is particularly low after adjustment for differences in family income.(JAMA. 1993;270:2464-2468)
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Cigarette smoking is a particularly pernicious behavior because of its high prevalence and mortality risk. We use the powerful methodology of life tables with covariates and employ the National Health Interview Survey-Multiple Cause of Death file to illuminate the interrelations of smoking with other risk factors, and with the combined influences of smoking prevalence and population size on smoking-attributable mortality. We find that the smoking-mortality gap is only modestly affected by other risk factors and excess deaths due to smoking among U.S. adults in the year 2000 were as great as 340,000. Better knowledge of the prevalence and mortality risk associated with cigarette smoking statuses enhances the future health and longevity prospects of the U.S. population.
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A debate within the mortality literature centers around the impact of health behaviors on the prospects of disadvantaged groups. Meanwhile, a growing body of work illustrates the social processes that shape changes in smoking levels by socioeconomic status (SES), especially educational attainment. These literatures are merged by examining the mediating effects of cigarette smoking on education gaps in U.S. adult mortality by age and gender. Findings reveal that cigarette smoking is an important mediator of the education-mortality gap for all males and for younger females. In particular, education-mortality gaps for young men narrow considerably when cigarette smoking is accounted for, while older women experienced no reduction in the education-mortality gap with controls for smoking. These results are consistent with diffusion arguments that describe SES differences in smoking adoption by age and gender and provide strong evidence that smoking is an important differentiator of mortality risks by education.
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Sumario: Analytical approaches and frameworks -- Patterns of mortality change -- Differential mortality -- Policy and programme implications
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A great deal of research has focused on factors that may contribute to the Hispanic mortality paradox in the United States. In this paper, we examine the role of the salmon bias hypothesis - the selective return of less-healthy Hispanics to their country of birth - on mortality at ages 65 and above. These analyses are based on data drawn from the Master Beneficiary Record and NUMIDENT data files of the Social Security Administration. These data provide the first direct evidence regarding the effect of salmon bias on the Hispanic mortality advantage. Although we confirm the existence of salmon bias, it is of too small a magnitude to be a primary explanation for the lower mortality of Hispanic than NH white primary social security beneficiaries. Longitudinal surveys that follow individuals in and out of the United States are needed to further explore the role of migration in the health and mortality of foreign-born US residents and factors that contribute to the Hispanic mortality paradox.