African-Americans, Puerto Ricans, and Mexican

African-Americans, Puerto Ricans, and Mexican

The University of Toledo
The University of Toledo Digital Repository
Master’s and Doctoral Projects
2009
Factors affecting asthma in minorities : AfricanAmericans, Puerto Ricans, and Mexican-Americans
Fouad Malik
The University of Toledo
Follow this and additional works at: http://utdr.utoledo.edu/graduate-projects
Recommended Citation
Malik, Fouad, "Factors affecting asthma in minorities : African-Americans, Puerto Ricans, and Mexican-Americans" (2009). Master’s
and Doctoral Projects. 361.
http://utdr.utoledo.edu/graduate-projects/361
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Factors affecting asthma in minorities:
African-Americans, Puerto Ricans, and Mexican-Americans
Fouad Malik
The University of Toledo
2009
ii
Acknowledgements
Lorraine Kenter – For her guidance in writing this paper
Amena Malik – For providing moral support while this paper was being written
My family – Also for providing moral support while this paper was being written
iii
Table of Contents
Introduction ......................................................................................................................................1
Etiology ............................................................................................................................................1
Triggers ............................................................................................................................................3
Problem Statement ...........................................................................................................................4
Purpose.............................................................................................................................................6
Research Questions ..........................................................................................................................6
Design ..............................................................................................................................................7
Literature Review.............................................................................................................................8
African-Americans ...........................................................................................................................8
Latinos............................................................................................................................................18
Puerto Ricans .................................................................................................................................18
Mexican-Americans .......................................................................................................................22
Discussion ......................................................................................................................................26
Conclusions ....................................................................................................................................31
Future Research .............................................................................................................................34
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Figures
Figure 1: Race among all asthmatics in the United States in 2001
Figure 2: Prevalence of asthma within each race in 2001
Figure 3: Overweight females, by race
Figure 4: Comparison of asthma prevalence for racial groups to the national average
Figure 5: Poverty, by race
Figure 6: FEV1 response, following bronchodilator use, in those with an FEV1 less than 80%, by
race
1 Introduction
Asthma is a chronic, or frequently recurring, condition of the lungs that can affect anyone
of any race, gender, or age. It is characterized by inflammation of the respiratory tract, with
hyperresponsive bronchoconstriction due to specific irritants that would not occur in normal
subjects. Finally, there are recurrent episodes of obstruction in the airway, due to inflammation
and hyperresponsive bronchoconstriction, that resolve spontaneously or with treatment
(Goldman & Ausiello, 2008). These irritants include pollen, dust, animal dander, pollution,
exercise, cigarette smoke, cold, and stress among others. According to the American Lung
Association (ALA), Asthma is the leading chronic illness of children in the US. Analysis of data
from the Centers for Disease Control (CDC), by the ALA in 2007, shows that approximately
34.1 million people have, at some point in their lives, been diagnosed with asthma. This problem
has been on the rise since the early 1980s (American Lung Association, 2008). In the US,
between 1982 and 1996, asthma prevalence increased by 59% (American Lung Association,
2008). Since 2001, asthma prevalence has increased by six percent (American Lung
Association, 2008). It’s estimated that in 2007 the direct cost of asthma, including hospital care,
physician services, prescription drugs, home health care, and nursing home care amounted to
$14.7 billion. That figure rose to $19.7 billion with the addition of other indirect costs of
asthma, such as lost productivity (National Heart Lung and Blood Institute, 2007).
Etiology
According to Fauci, Braunwald, et al., risk factors for asthma can be broken down into
two categories. Endogenous factors such as atopy, airway hyperresponsiveness, gender, genetic
predisposition, and ethnicity can increase susceptibility for asthma. Exogenous or environmental
2
factors including indoor and outdoor allergens, passive smoking, respiratory infections, and
occupational sensitizers increase susceptibility to asthma. Obesity and early viral infections are
possible exogenous factors that increase susceptibility to asthma (Fauci et al., 2008, pp. 15961597).
Atopy, a major endogenous risk factor, is characterized by allergic reactions to
environmental triggers, such as dust mites, animal fur, cockroaches, grass and tree pollen, which
cause an increase in IgE. In susceptible individuals this increase in IgE leads to eczema, allergic
rhinitis, or asthma. Studies have shown that only a portion of those with atopy develop asthma,
suggesting that among those with atopy, other genetic or environmental factors predispose many
to asthma. Genetics is suggested to be a factor in the presence of asthma as well as severity of
the disease (Sarafino & Goldfedder, 1995). Many genes have been implicated in the onset of
asthma; according to Fauci, Braunwald, et al., genes for Interleukins (IL) 4, 5, 9, and 13 of T
helper 2 (TH2) cells have been associated with atopy, and eventually asthma. Genes that are
directly thought to be responsible for asthma include DPP-10, GPRA, ADAM-33, and ORMDL3
(Fauci et al., 2008, p. 1597; Galanter et al., 2008).
Among environmental factors, viral infections are thought to be a risk factor for the onset
and exacerbations of asthma (Heymann et al., 2004). A 2004 study looked at children two to
eighteen years of age that were hospitalized for wheezing. For those under the age of three, viral
infections where shown to be the major risk factor for wheezing (Heymann et al., 2004). Two
such viruses are thought to be respiratory syncytial virus (RSV) and rhinovirus (RV) (Hansbro,
Horvat, Wark, & Hansbro, 2008). Air pollution is an important factor in exacerbations of
asthma, but its role as an etiology of asthma is much less certain. Cities with higher levels of
ambient traffic pollution have about the same prevalence of asthma as rural areas, which have
3
lower levels of pollution (Fauci et al., 2008, p. 1597). Stress has also been linked to asthma, as
evident in a study that showed increased morbidity from asthma in an inner-city neighborhood
with an increased level of community violence (Wright, Mitchell et al., 2004). Other
environmental agents, such as occupational agents, inhaled allergens, age of mother, duration of
breast feeding, premature birth or low birth weight, and inactivity, have been associated with
asthma (Fauci et al., 2008, p. 1597).
Understanding the etiology of asthma is paramount in attempting to lower its burden.
Prevention of potential etiologies could help lower asthma morbidity or exacerbations. Reducing
maternal smoking, while pregnant and post-partum, as well as lowering air pollution or allergens
in the home due to animals could all potentially lower the morbidity of asthma. Though gender,
ethnicity and genetic predisposition are etiologies that cannot be controlled, the burden of asthma
can be reduced by understanding their role in asthmatics. Based on variations of the gene
ADRβ2, African-Americans do not respond well to β2-agonists, a mainstay in the treatment of
asthma, thus another treatment should be considered (Hawkins et al., 2006).
Triggers
Triggers that lead to bouts of asthma vary. Allergens, like house dust mites, cats,
cockroaches, grass pollen, and tree pollen, lead to activation of mast cells, releasing
bronchoconstriction mediators. Pharmacological agents such as β-blockers, used for
hypertension and arrhythmias, are often triggers for asthma. Aspirin is another pharmacological
agent that can act as an asthma trigger. Aspirin induced asthma (AIA) is a condition which
includes asthma, chronic rhinosinusitis, and nasal polyps (Berges-Gimeno, Simon, & Stevenson,
2002). Hyperventilation, which occurs during exercise, causes changes in osmolality of the fluid
4
lining the airway. These changes activate mast cells, inducing bronchoconstriction through
chemical mediators. Cold air can induce asthma attacks by this same mechanism. Hormones
play a part in triggering asthma in females, possibly due to a fall in progesterone levels prior to
menstruation (Fauci et al., 2008, p. 1601). Viral infections, like RSV and RV, air pollution, and
occupational exposures are possible etiologies for asthma but are also triggers in susceptible
asthmatics.
Problem Statement
Asthma is a chronic disease that has many consequences. In 2003, it accounted for 12.8
million missed school days (Akinbami, 2006). A study of almost 500 asthmatics showed that
sleep quality was impaired substantially in even mild-moderate asthmatics with asthma control
improving sleep quality (Mastronarde, Wise, Shade, Olopade, & Scharf, 2008). Reduced sleep
lowered the quality of life for asthmatics more than their asthma symptoms alone. Additionally,
metastases of skin, colorectal, and breast cancer to the lungs have been associated with allergic
respiratory inflammation (Taranova et al., 2008). In a study of over four hundred pregnancies,
asthma exacerbations in the first trimester were found to significantly increase the risk of having
a child with congenital malformations (Blais & Forget, 2008). Blais and Forget believe that
maternal hypoxia and respiratory alkalosis, seen in acute asthma attacks, can decrease delivery of
blood oxygen to the fetus, leading to malformations (Blais & Forget, 2008). Further,
uncontrolled asthma will cause damage to the lungs and worsening of symptoms, leading to
more severe symptoms, hospitalization from asthma attacks, or even death. It is estimated that
about one in every two hundred fifty deaths worldwide is due to asthma (Masoli, Fabian, Holt, &
Beasley, 2004).
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Asthma affects people of all races, gender, and age; it is more common in AfricanAmericans and Puerto Ricans (American Lung Association, 2007). In 2001, white Americans
represented 72.10% of all asthmatics and African-Americans comprised only 13.47% (figure 1).
However, CDC data analysis by the ALA, shows that African-Americans have a higher
prevalence of asthma than the majority white population (American Lung Association, 2007), as
demonstrated by white Americans having a 10.69% prevalence of asthma and AfricanAmericans having 12.19% asthma prevalence (figure 2). Hispanics, in general, have a lower
prevalence of asthma than the white population. Mexican-Americans have the lowest prevalence
of asthma when compared to all races, with only Asian-Americans having a lower prevalence of
asthma. Puerto Ricans have a higher prevalence of asthma, at 24.5% (figure 2), than even
African-Americans (American Lung Association, 2007).
African-Americans and Puerto Ricans often suffer from a more severe form of asthma
(Bai, Hillemeier, & Lengerich, 2007). African-American children hospitalized for asthma in
Pennsylvania were found to have severe asthma more often than hospitalized white children (Bai
et al., 2007). Hispanic children had fewer cases of severe asthma than white children, though
Hispanic children only accounted for 1.5% of the study sample (Bai et al., 2007). Analysis of
data from the 1994-1995 National Health Interview Survey, by Newacheck and Halfon, found a
three-fold increase in disability, for children, due to asthma in the past quarter century. AfricanAmerican children had a higher incidence of disability due to their asthma than white children,
even after controlling for sociodemographic variables such as family income or family structure
(Newacheck & Halfon, 2000). According to CDC data, from 2001 through 2003, AfricanAmericans had higher death rates due to asthma than whites (Moorman et al., 2007). This held
true for both genders and all age groups (Moorman et al., 2007).
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Mexican-Americans have among the lowest prevalence of asthma of any minority in the
U.S. (American Lung Association, 2007). Yet, it has been shown that those born in the U.S.
have a higher prevalence of asthma than those born in Mexico (Eldeirawi, McConnell, Freels, &
Persky, 2005).
Purpose
The purpose of this paper is to point out some of the etiologies of asthma, genetic and
environmental factors, and differences in diagnosis and/or treatment in African-Americans,
Puerto Ricans, and Mexican-Americans. This paper correlates the etiology, genetics,
environmental factors, and differences in diagnosing and/or treating asthma, with asthma
prevalence, hospitalizations, morbidity, mortality, and severity of symptoms in these select
minorities.
Research Questions
What role does genetics play in the development or triggering of asthma in African-Americans,
Puerto Ricans, and Mexican-Americans?
What role does an individual’s environment play in development or triggering of asthma in
African-Americans, Puerto Ricans, and Mexican-Americans?
Is asthma diagnosed or treated differently in African-Americans, Puerto Ricans, or MexicanAmericans?
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Design
To accomplish this, a review of literature, from 1993 through 2008 will be utilized, plus
select sentinel articles. Search terms used: African-Americans and asthma, asthma and Latinos,
Hispanic Americans and asthma. Databases used: PubMed, OhioLINK Database, and Wayne
State University Online Journals.
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Literature Review
African-Americans
In 2004, over fourteen million adults and six million children in the United States had
asthma. A disproportionally large number of these asthmatics were African-American.
According to ALA calculations of data from the National Health Interview Survey (NHIS), in
2004, African-Americans had an 11.5% higher prevalence of asthma than whites (American
Lung Association 2007). While African-Americans represent only 12.1% of the population of
the United States, they represent 25% of the asthmatic deaths. In 2007, African-American
children were nearly four times more likely to be hospitalized for asthma than white children
(US Department of Health and Human Services, 2007). African-Americans also have higher
rates of death due to asthma than whites, who make up the majority of the population of the
United States (US Census Bureau, 2007), in all gender and age categories (Moorman et al.,
2007).
According to many researchers, asthma has an effect on pregnant African-Americans.
Carroll, Griffin et al. found that all pregnant, low-income women required emergency
department (ED) visits, needed rescue corticosteroids, and were hospitalized due to their asthma
more often than other pregnant women (Carroll et al., 2005); this relationship continued for lowincome pregnant African-American women when compared to low-income pregnant white
women (Carroll et al., 2005). Asthma during pregnancy does not only affect the mother, but it
can affect the child as well (MacMullen, Tymkow, & Shen, 2006). Ehrenthal, Jurkovitz et al.
found that pregnant African-American women had higher rates of premature birth and low birth
weight (LBW) babies when compared to all others ethnicities (Ehrenthal, Jurkovitz, Hoffman,
Kroelinger, & Weintraub, 2007). In the preceding study, asthma and black race were risk factors
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for premature birth, yet asthma and black race, along with other health problems, could not fully
account for higher rates of prematurity and LBW (Ehrenthal et al., 2007).
It is thought that the environment plays a large role in asthma and controlling
environmental factors can help in managing asthma (American Lung Association, 2008). An
environmental factor, for African-Americans, that contributes to asthma is place of residence,
meaning urban vs. non-urban housing, and the conditions of the neighborhood in which one lives
(Friedman & Rosenbaum, 2004). Friedman found that throughout the U.S., African-American
houses are often of lower quality than white American houses (2004). In New York City, the
highest rates of asthma were seen in African-American and Puerto Rican families (Rosenbaum,
2008). After controlling for deteriorating housing conditions and perceptions of low social
cohesion, prevalence of asthma in African-Americans and Puerto Ricans was similar to that seen
in whites (Rosenbaum, 2008), showing that environmental factors such as deteriorating housing
conditions and perceptions of low social cohesion increase incidence of asthma in these groups.
Rosenbaum suggests that in addition to environmental factors associated with deteriorating
housing conditions, stress from “discrimination in the housing market” also contributes to higher
levels of asthma in African-Americans and Puerto Ricans (Rosenbaum, 2008). In urban settings,
such as Harlem, asthma is more prevalent and more severe (Nicholas et al., 2005). In 2005
Nicholas et al. reported that children in Harlem had four times the prevalence of asthma as the
national average.
The effect of socioeconomic status (SES) has often been studied in association with
asthma. In the Jackson Heart Study, a study of only African-Americans, prevalence of asthma
was lower than the general African-American population (Hickson, Wilhite, Petrini, White, &
Burchfiel, 2009). Hickson’s explanation for the lower prevalence of asthma in the Jackson Heart
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Study was that the subjects generally had a higher SES. Women, in the Jackson Heart Study
were found to have a higher prevalence of asthma than men (Hickson et al., 2009). This
disparity was attributed to higher amounts of stress, worse perceived general health, and lower
education attainment, which could be factors of low SES (Hickson et al., 2009). In looking at
mortality rates from asthma in the U.S., Grant et al. found that African-Americans had higher
asthma related mortality than whites, that low education led to higher asthma mortality than
higher education, and that low income was associated with higher asthma mortality than higher
income (Grant, Lyttle, & Weiss, 2000). The previous study showed that black race/ethnicity was
associated with higher asthma mortality, independent of SES (Grant et al., 2000); yet, Grant et al.
concluded that both black race/ethnicity and low SES were independently associated with high
asthma mortality (Grant et al., 2000). Smith et al. have also shown a potential for SES being
associated with asthma in African-Americans (Smith, Hatcher-Ross, Wertheimer, & Kahn,
2005). African-American children have a greater risk of asthma than white children, but only
among the very poor, showing that environmental factors, such as SES, have a greater impact on
asthma than genetics (Smith et al., 2005).
Roberts showed that African-American children, one to five years old, had a higher
prevalence of asthma and hospitalization from asthma than whites and Mexican-Americans; yet
income, a factor of SES, did not have much impact on the higher prevalence of asthma (Roberts,
2002). Like Roberts (2002), Stingone and Claudio also demonstrated higher rates of ED visits
and hospitalizations due to asthma in African-Americans when compared to whites (2006).
Stingone and Claudio, as well as Erickson et al., found no correlation between these increased
rates of ED visits and hospitalizations and SES (2006: 2007). While studying cohorts of
African-American and white subjects on similar healthcare plans, Erickson et al. found that
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African-American subjects, typically, were hospitalized more often and had more ED visits due
to asthma than their white counterparts (2007). These differences were not explained by SES,
asthma severity, and asthma therapy though Erickson et al. state that there may have been other
socioeconomic factors that they did not take into account (Erickson, Iribarren, Tolstykh, Blanc,
& Eisner, 2007).
Stevenson et al., in a study of indoor allergen sensitivity among children in the US, found
that African-American children are more likely to be sensitive to allergens, than white children,
showing that disparities in allergen sensitivity were consistent with disparities in asthma
morbidity between African-Americans and whites (2001). African-American children were
more than twice as likely to be sensitive to Alternaria alternata, an opportunistic pathogen and
asthma-causing indoor allergen, as white children (Stevenson et al., 2001); African-American
children were more likely to be sensitive to dust mite allergen, and cockroach antigen, all of
which have long been associated with allergic asthma (Kang, 1976), than white children
(Stevenson et al., 2001).
Stress is another potential factor that predisposes African-Americans to asthma (Wright,
Mitchell et al., 2004). While studying the effect of community violence on asthma morbidity, in
2004, Wright et al. found inner-city families to have a higher prevalence of exposure to violence,
stating that “exposure to violence was independently associated with asthma morbidity.” The
effect of neighborhood violence on asthma morbidity was at least partly due to stress (Wright,
Mitchell et al., 2004). Caretaker behaviors such as keeping children indoors, smoking, and
skipping medications are often exhibited during stress and are partly to blame for the morbidity
of asthma (Wright, Finn et al., 2004). One explanation of why chronic caregiver stress increases
asthma morbidity is higher levels of total IgE expression, leading Wright et al. to believe that, in
12
susceptible children, stress during early life can result in changes in immune reactivity, which
can initiate an immune response. This increase in IgE levels occurs during a time of T-cell
maturation, when exposure to allergens and the environment can have a large influence on a
child’s atopic phenotype (Wright, Finn et al., 2004). The correlation between asthma and IgE
expression is supported by Wright et al, who associated caregiver stress, early in a child’s life,
with risk of wheezing (Wright, Cohen, Carey, Weiss, & Gold, 2002). This association persisted
even after adjusting for maternal smoking, lower respiratory illnesses, allergen levels, and breastfeeding (Wright et al., 2002). A possible alternative explanation is that chronic stress leaves an
individual at a higher susceptibility for respiratory infections from agents such as RV (Cohen et
al., 1998).
In the United States, Mexican-American and African-American adolescents have a high
prevalence of overweight (Ogden, Flegal, Carroll, & Johnson, 2002). Being overweight, these
Mexican-Americans and African-Americans are more susceptible to conditions associated with
obesity, such as asthma. Rodriquez et al. associated obesity with asthma (2002), finding that
children with a BMI greater than the 85th percentile had 1.94 times the likelihood of having a
current asthma diagnosis than those with BMI’s less than the 85th percentile (Rodriguez,
Winkleby, Ahn, Sundquist, & Kraemer, 2002).
Overweight and obesity are also more common in African-American women; from 2001
through 2004, the CDC found that 79.5% of African-American women over the age of 20 were
overweight or obese versus 57.1% of non-Hispanic white women (figure 3). Coogan et al.,
hypothesized that body mass index (BMI) was positively associated with adult-onset asthma in
African-American women (Coogan, Palmer, O'Connor, & Rosenberg, 2009); they then tested
this hypothesis by following a large cohort of African-American women, 21 to 69 years old, for
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ten years (Coogan et al., 2009). Questionnaires elicited information about participant
demographics and lifestyle factors, height and weight, diet, reproductive history and medical
conditions at baseline, in 1995. Participants also completed a follow-up questionnaire every
second year for five cycles. After excluding participants with previous bariatric surgeries, lung
cancer, diagnosis of asthma prior to 1996, pregnancy at baseline, any cancer in the follow-up
period, or missing information about smoking or BMI at baseline, 46,435 women remained.
Researchers, in this study, relied on questions asking about physician-diagnosed asthma and use
of asthma medications to determine asthma status. These questions are a perfectly suitable
method of determining asthma status, instead of examining each patient clinically, as
questionnaires have been recommended as the preferred assessment of asthma in such large
cohort studies and have been used in most similar studies (Burr, 1992). Results showed that
BMI was associated with asthma in all groups and subgroups of age, energy intake, energy
expenditure, presence of sleep apnea, smoking history, parental history of asthma, and BMI at
eighteen years old. Severely obese (BMI > 40) women had nearly a three-fold greater incidence
of asthma than women with a BMI of 20 to 24 (Coogan et al., 2009). More importantly, asthma
risk increased in association with increases in BMI (Coogan et al., 2009). Change in weight
from eighteen years old was positively associated with risk of asthma, especially in those who
gained fifteen kilograms or more (Coogan et al., 2009). Data from the Third National Health and
Nutrition Examination Survey showed similar increases in asthma prevalence with increases in
BMI, in those four to seventeen years old, even after controlling for gender, age, ethnicity,
smoke exposure, household size, birth weight, and whether they were breast-fed. Ethnicity or
gender did not change the association between asthma and BMI (von Mutius, Schwartz, Neas,
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Dockery, & Weiss, 2001). Von Mutius et al. suggest that lower tidal lung volumes in overweight
individuals may be responsible for this increase in asthma (2001).
African-Americans have been shown to report asthma symptoms differently than the
general population (Trochtenberg, BeLue, Piphus, & Washington, 2008). African-Americans are
less likely to report night-time asthma symptoms and are also less likely to complain of dyspnea,
which is an indicator of asthma control (Trochtenberg et al., 2008). Inadequately reporting
symptoms can lead to potential consequences, such as under-treatment or increased morbidity
and mortality of asthma in this minority (Trochtenberg et al., 2008). By not reporting or
perceiving nocturnal asthma symptoms or dyspnea, African-Americans are misdiagnosed as
being stable asthmatics while their asthma is actually unstable (Trochtenberg et al., 2008).
According to Trochtenberg et al., this might help to explain some disparities in asthma treatment
and asthma outcomes that are seen in African-Americans.
When African-Americans and whites visit the ED with asthma exacerbations of similar
severity, similar doses of anti-inflammatory medications were prescribed, even though AfricanAmericans had higher rates of ED visits (Boudreaux, Emond, Clark, & Camargo, 2003).
Further, Boudreaux et al. found that, though whites and African-Americans were prescribed the
same anti-inflammatory medications, African-Americans were found to use these less frequently
before going to the ED (2003), which would lead to worse asthma outcomes. However, Wright
demonstrated the opposite in studying medication use in asthmatic children in California, by
showing an association between black race and use of prescription medication (2007). In this
study, African-Americans were twice as likely to report having taken prescription medications
for asthma (Wright, 2007). Yet others have seen no association between medication use and
race/ethnicity (Erickson et al., 2007). No matter how much African-Americans use medications
15
to control asthma they often do not see much benefit from these medications. For MexicanAmericans and Puerto Ricans, use of inhaled corticosteroids increases their responsiveness to
short acting β-agonists (Naqvi et al., 2008). African-Americans did not receive these same
benefits from inhaled corticosteroids (Naqvi et al., 2008).
Another potential reason for higher prevalence of asthma in African-Americans is
overdiagnosis (Roberts, 2002). In one study, African-Americans had a 76% greater chance, than
whites, of being diagnosed with asthma versus possible asthma (Shalowitz, Sadowski, Kumar,
Weiss, & Shannon, 2007). Roberts also showed that African-Americans were overdiagnosed
with asthma, even when presenting with similar symptoms as other children (Roberts, 2002).
African-Americans are more likely to have severe asthma, a lower quality of life due to
their asthma, problems controlling asthma, greater number of ED visits due to asthma and be
prescribed three or more long-term controllers (Haselkorn, Lee, Mink, & Weiss, 2008; Vargas et
al., 2006). Although factors such as health coverage, treatment settings, IgE levels, and BMI
influenced severity of asthma, they do not fully explain disproportionate levels of asthma in
African-Americans (Haselkorn et al., 2008). In the Study of African Americans, Asthma, Genes,
and Environments (SAGE), based on pre- FEV1 or baseline FEV1, Tsai et al. showed that
African ancestry was associated with more severe asthma (Tsai et al., 2006). Analysis of
National Health Interview Survey data from 1997 through 2003 showed that African-American
children had more ED visits for asthma than comparable white children (McDaniel, Paxson, &
Waldfogel, 2006). McDaniel et al. suggest that the reason for this is due to more severe asthma
in African-Americans (2006).
Multiple genes within the human genome are associated with asthma (Barnes, Grant,
Hansel, Gao, & Dunston, 2007). One such gene, CASP10, has been shown to modify airway
16
obstruction in African-American and white Americans with asthma (Smith et al., 2008).
Associated with a severe form of asthma in African-Americans, Myosin Light Chain Kinase
(MLCK), encoded by the MYLK gene, plays a key role in contractions of endothelium and
smooth muscle (Flores, Ma, Maresso, Ober, & Garcia, 2007). In a study of 302 unrelated asthma
cases, seventeen alleles of this gene were found (Flores et al., 2007). One of these alleles,
Pro147Ser, is common in African Americans but not other races or ethnicities, and is associated
with an increased susceptibility for severe asthma in African-Americans (Flores et al., 2007).
Another gene that has been shown to play a role in asthma in African-Americans is the
KCNMB1 gene, which controls voltage-gated K+ (BK) channels in airway smooth muscle. The
818T allele of this gene, which is specific to African-Americans, was associated with a 13%
decline in FEV1. This decline in FEV1 only occurred within males in the sample. The authors of
the previous study believe that estrogen and estradiol afford protection, via upregulation of BK
channels, to females with this allele (Seibold et al., 2008). ICAM-1, or Intercellular adhesion
molecule-1, is yet another gene involved in airway hyperresponsiveness and airway
inflammations (Li et al., 2005). Li et al. associated variations of this gene with a lower risk of
asthma in whites, African-Americans, and Hispanics (2005).
Not only is genetics an important factor in predicting the severity of asthma in AfricanAmericans (Hawkins et al., 2006), but it also influences treatment of asthma. Hawkins et al.
found differences in lung function and β2-agonist responsiveness based on variations in the
ADRβ2 gene, especially in African-Americans (2006). It is suggested by Hawkins et al. that
these variations in ADRβ2 may also be responsible for possible adverse effects associated with
chronic use of β2-agonists, such as death (2006).
17
It is clear that African-Americans suffer from higher asthma prevalence, hospitalizations,
morbidity, and mortality than the general population of the United States (American Lung
Association, 2007). Environmental factors, the way asthma is diagnosed and/or treated, quality
of care, and genetic factors all influence asthma in African-Americans.
18
Latinos
As in African-Americans, asthma is a problem in Latinos living in the United States;
however, unlike African-Americans, Latinos have a lower prevalence of asthma than white
Americans (American Lung Association, 2007). Two subgroups from the Latino minority
population are of special interest. Puerto Ricans have the highest prevalence of asthma in the
US. Conversely, Mexican-Americans have the second lowest prevalence of asthma in the US,
with only Asian-Americans being lower (American Lung Association, 2007). Puerto Ricans
have 56% higher prevalence of asthma than the general population, while Mexican-Americans
have 62% lower prevalence of asthma than the general population (figure 4). Among Puerto
Ricans and Mexican-Americans, genetics may play a different role in asthma. According to the
Collaborative Study on the Genetics of Asthma, different genes influence asthma in specific
races ("A genome-wide search," 1997). This genetic variation between races may help to
explain differing rates of asthma in these populations ("A genome-wide search," 1997).
Puerto Ricans
Puerto Ricans have the highest prevalence of asthma in the US (American Lung
Association, 2007; Rose, Mannino, & Leaderer, 2006), and have higher mortality from asthma
than other Latinos, African-Americans, and whites (Homa, Mannino, & Lara, 2000). Puerto
Ricans, when compared to African-Americans are more likely to have severe asthma, yet have
less lengthy hospital stays resulting from asthma exacerbations (Cohen et al., 2006). Cohen,
Celedon et al. also found that Puerto Ricans were more likely to see a physician for their asthma
than African-Americans, suggesting that more outpatient physician visits would make Puerto
Ricans less likely to have severe asthma exacerbations (2006).
19
As with asthma in the general population, environment plays a role in asthma for Puerto
Ricans. According to CDC statistics, Puerto Ricans have higher rates of smoking than the
general population ("Prevalence of cigarette use," 2004). Among fourteen race/ethnic
populations studied, Puerto Ricans had the second highest rates of smoking, with only American
Indian/Native Americans having higher rates ("Prevalence of cigarette use," 2004). Though
Puerto Ricans had marginally higher rates of smoking than other races, it remains a possible
contributor to increased prevalence of asthma in Puerto Ricans ("Prevalence of cigarette use,"
2004).
Latinos often have lower SES than the general population. In 2001, 21.4% of Latinos
lived below the poverty line, compared to 7.8% of the white population (figure 5). Of these
Latinos, Puerto Ricans had the highest rate of living below the poverty line, at 26.1% (Roberto
R. Ramirez & G. Patricia de la Cruz, 2003). The impact of SES on asthma in Puerto Ricans is
debatable. A study of ten racial/ethnic groups in New York City showed that perceptions of low
social cohesion and deteriorating housing conditions were responsible for increased prevalence
of asthma in Puerto Ricans (Rosenbaum, 2008). Beckett et al. (1996) and Claudio et al. (2006)
showed that SES does not have a significant effect on asthma in Puerto Ricans. According to
Claudio et al., children in New York City, living in areas of lower SES, had a 70% greater
chance of having asthma than comparable children living in areas of higher SES; this was true
for all races except Puerto Ricans (2006). Puerto Ricans had increased rates of asthma regardless
of high or low SES (Claudio, Stingone, & Godbold, 2006). Lara et al. found that Puerto Rican
children had similar socioeconomic characteristics to African-American children (2006). Yet,
prevalence for asthma was still higher for Puerto Ricans than African-Americans (Lara,
Akinbami, Flores, & Morgenstern, 2006).
20
Findley et al. found that more Puerto Rican families had very low income than any other
ethnicity; however, income and socioeconomic status were not associated with asthma in this
study (2003). Unlike the rest of the study subjects who were sensitive to cockroach antigen,
there was no association seen between cockroach antigen and asthma for Puerto Rican children
despite Puerto Ricans having higher reports of cockroaches in the home (Findley et al., 2003).
Findley et al. admit that Puerto Ricans may report cockroaches in the home differently than
others, due to cultural differences. However association was seen between rats and mice in the
home and asthma in the Puerto Rican sample (Findley et al., 2003). Others have also associated
mold in the home, environmental tobacco smoke, pesticides, and cockroaches with asthma
diagnosis (Freeman, Schneider, & McGarvey, 2003a).
Interestingly, prevalence of asthma and hospitalizations from asthma are lower for Puerto
Ricans living on the mainland than those living on the island of Puerto Rico (Cohen et al., 2007;
Lara et al., 2006). A possible explanation cited by Cohen et al. is that temperature, air pollution,
humidity, and exposure to Blomia tropicalis, a dust mite, have a large influence on asthma in
tropical locations such as Puerto Rico (Arruda et al., 1997). Another explanation cited by Cohen
et al. is a genetic predisposition for severe asthma among all Puerto Ricans (Choudhry et al.,
2005). Conversely, others have found that Puerto Ricans born on the mainland had a similar
prevalence of asthma as island born Puerto Ricans (Dumanovsky & Matte, 2007).
Genetics exerts a large influence on asthma in Puerto Ricans as evidenced by
responsiveness to albuterol. In comparing bronchodilator responsiveness among AfricanAmericans, Mexican-Americans, and Puerto Ricans, Naqvi et al. showed that African-American
children with moderate-to-severe asthma, and Puerto Ricans of all ages, had among the lowest
responsiveness to bronchodilators (2007). Puerto Ricans had an FEV1 improvement of 4.8%
21
after bronchodilator use, whereas African-Americans had an improvement of 7.0% (Naqvi et al.,
2007). In asthmatics with an FEV1 of less than 80%, Puerto Ricans had an FEV1 improvement
of 8%, while African-Americans had an improvement of 14.7% (figure 6). Naqvi et al. found
that ethnicity was a more significant factor than socioeconomic status or medication use in lower
response to albuterol (Naqvi et al., 2007). Potential explanations for this could be that asthma in
Puerto Ricans might not involve as much bronchospasms, which would reduce the effectiveness
of albuterol (Burchard et al., 2004). Burchard et al. propose that asthma in Puerto Ricans could
be associated with more impairment in relaxation of airway smooth muscle, greater airway
remodeling, greater downregulation of β2-receptors, or other differences in polymorphism of
proteins that are involved in the β2-receptor pathway (2004).
Akinbami et al. examined whether asthma was underdiagnosed among minority children
and came to the conclusion that minority children with asthma symptoms were not
underdiagnosed (2005). In the previous study it is reported that Puerto Ricans have much higher
rates of asthma diagnosis than most other nationalities (Akinbami, Rhodes, & Lara, 2005).
Analyzing the previous study, Hunningshake et al. hypothesize that greater rates of asthma
diagnosis could be due to differences is severity of asthma between Puerto Ricans and nonHispanics (2006). Hunningshake et al. also state that the possibility of overdiagnosis in Puerto
Ricans cannot be ruled out (2006).
22
Mexican-Americans
Among minorities, Mexican-Americans have among the lowest rates of asthma in the US
(American Lung Association, 2007; Davis, Kreutzer, Lipsett, King, & Shaikh, 2006). MexicanAmericans are similar to Puerto Ricans in that both have mainly European, African, and Native
American ancestry (Salari et al., 2005). For Mexican-Americans, ancestry consists of 51.7%
Native American, 44.9% European, and 3.4% African ancestry (Salari et al., 2005). Analysis of
the GALA study by Salari et al. showed that European ancestry was associated with more severe
asthma (Salari et al., 2005). Risk for severe asthma increased by 37% with each 10% increase in
European ancestry (Salari et al., 2005). Conversely, Native American ancestry was associated
with milder asthma (Salari et al., 2005). Also, no association was seen, in this study, linking
African ancestry and severity of asthma (Salari et al., 2005). Is there then a single gene that
leads to susceptibility to asthma in this population? It seems unlikely (Holberg, Halonen,
Wright, & Martinez, 1999). Holberg et al. investigated the inheritance of asthma in Latinos and
whites in Tuscon, AZ and were not able to find a single locus, two-allele gene that was
responsible for asthma (Holberg et al., 1999). Holberg et al. hypothesized that inheritance of
asthma was based on a polygenic or oligogenic mode of inheritance (1996; 1999). This mode of
inheritance was seen for both Mexican-Americans and whites (Holberg et al., 1999).
Despite a low prevalence of asthma, Mexican-Americans born and raised in the US are
diagnosed with asthma more frequently than those born in Mexico (Martin et al., 2007). Salari et
al. showed that this could possibly be due to the genetic background of those born the in the US
(2005), while Cagney et al. proposed that it could be due to stress (2007). While studying
asthma in Chicago neighborhoods, Cagney et al. found that the lower level of asthma in foreignborn Latinos was dependant on community-level factors (2007). In his previous study, Cagney
23
et al. showed that when living in a neighborhood with a high presence of foreign-born Latinos,
asthma prevalence was lower (Cagney, Browning, & Wallace, 2007). An earlier study by
Cagney and Browning found that collective efficacy, a measure of neighborhood trust and
attachment, was associated with lower levels of asthma and other respiratory illnesses (2004).
Analysis of data from the Third National Health and Nutrition Examination Survey found
that Mexican-Americans and African-Americans were more likely to be sensitized to indoor
allergens such as dust mites, cockroaches, and Alternaria alternata (Stevenson et al., 2001).
Other environmental factors associated with asthma in Mexican-Americans are mold in the home
and environmental tobacco smoke (Freeman et al., 2003a).
Acculturation, the process by which immigrants adopt the culture and way of living of
another group, may have a large influence on asthma in Mexican-Americans (Martin et al.,
2007). Despite having a lower SES, first-generation Mexican-Americans eat healthier than
second-generation Mexican-Americans (Gold & Acevedo-Garcia, 2005; Krebs & Jacobson,
2003). First-generation Mexican-American women have more proteins, Vitamin A and C,
calcium, and folic acid in their diets than second-generation Mexican-Americans (Guendelman
& Abrams, 1995). By adopting, an ‘American’ culture, Mexican-Americans may make bad
dietary decisions, such as consuming more fast food and soda, leading to obesity and the
consequences of obesity (Guendelman & Abrams, 1995). The diet of second-generation
Mexican-American women is closer to that of non-Hispanic white women than the diet of firstgeneration Mexican-Americans women (Guendelman & Abrams, 1995).
Mexican-American adolescents have higher rates of being overweight than the general
public (Ogden et al., 2002). This makes them more likely to have an asthma diagnosis
(Rodriguez et al., 2002). Rodriquez et al. found a strong association between BMI greater than
24
the 85th percentile and asthma, though only for children and adolescents (Rodriguez et al., 2002).
For adults forty years or older, prevalence of obesity was as high as fifty percent in one study of
Mexican-Americans living in Los Angeles (Torres, Azen, & Varma, 2006). Obesity in these
adults was also associated with asthma, hypertension, heart failure, angina, arthritis, back pain,
and diabetes (Torres et al., 2006).
Smoking, a suspected etiology of asthma, is associated with acculturation. According to
Unger et al. English language use, an indicator of acculturation was associated with an increased
lifetime risk of smoking among Hispanics (Unger et al., 2000). Those that spoke only English in
the home had two times the risk of smoking as those speaking primarily, or only speaking, a
different language (Unger et al., 2000).
Though US-born Mexican-Americans generally have better education, prenatal care, and
socioeconomic indicators, they are at a greater risk for preterm deliveries than Mexican-born
Mexican-Americans (Crump, Lipsky, & Mueller, 1999) because new immigrants tend to have
better birth outcomes than immigrants that have lived longer in the US (Crump et al., 1999). An
explanation for this is due to an earlier age of pregnancy, increased smoking or alcohol
consumption, or losing social support structures for U.S.-born Mexican-Americans (Crump et al.,
1999). With time, though, any protective advantage fades (Crump et al., 1999).
It stands to reason that U.S.-born Mexican-Americans would be more proficient English
speakers than Mexican-born Mexican-Americans. English proficiency should lead to lower rates
of asthma diagnoses because patients can better communicate their symptoms. The opposite is
also a possibility; that Mexican-born Mexican-Americans, who would prefer to speak Spanish,
may be uderdiagnosed because of an inability to correctly communicate asthma symptoms
(Shalowitz et al., 2007). It is also possible that newer immigrants, those that prefer to speak
25
Spanish, do not have equal access to healthcare as those that prefer to speak English (Shalowitz
et al., 2007).
Children, of all races, with health insurance are more frequently diagnosed with asthma
than those without insurance, found one study (Freeman, Schneider, & McGarvey, 2003b).
Mexican-American children generally have lower rates of health insurance than other children
(Freeman et al., 2003b; Wright, 2007); however, as insurance status improved for this group, so
did the diagnoses of asthma (Freeman et al., 2003b). Due to insufficient data, however, this
hypothesis could not be proven (Freeman et al., 2003b).
Martin et al. also found an association between acculturation and asthma prevalence in
Mexican-Americans, yet the effects of acculturation were not mediated by time spent in the U.S.
or language usage by Mexican-Americans (Martin et al., 2007). The effects of acculturation
were mediated more by birthplace in Mexico versus the U.S., caregiver education and marital
status, child insurance status, life stress, and social support (Martin et al., 2007).
26
Discussion
For African-Americans, housing conditions, living in an urban neighborhood, indoor
allergen sensitivity, perceived caregiver stress, neighborhood violence, maternal smoking, and
obesity have been shown to be associated with asthma. These variables are not independent of
each other; in many instances it is difficult to separate these variables. Housing in these urban
areas, often substandard, increases the likelihood of exposure to many asthma triggers, including
dust mites and cockroach antigen. Substandard conditions can increase caregiver stress. While
stress itself is associated with an increase in IgE levels (Wright, Finn et al., 2004), it has many
other consequences, possibly increasing the incidence of smoking among caregivers, which is
associated with asthma.
Asthma is more prevalent in the inner-city and in those that generally have a lower SES
(Nicholas et al., 2005). Even in middle-class asthmatics, a disparity remains in the prevalence of
asthma between African-American children and white children (Weitzman, Byrd, & Auinger,
1999). This disparity would suggest that race and genetics are contributing risk factors for
asthma in African-Americans.
The debate of how much SES impacts asthma in African-Americans is complex. Some
studies claim that that SES has a major impact on asthma disparities between African-Americans
and whites, while other studies find no evidence of an association between asthma and SES in
African-Americans. Often, researchers will find no correlation between disparities in asthma and
family income, a factor of SES. Though income may not have any effect on asthma, an
association between SES and asthma cannot be ruled out. Other factors associated with low
SES, such as an urban setting or stress, may have an effect. Those with low SES often live in an
urban, inner-city setting, which has been associated with asthma. The stress associated with a
27
low SES, such as neighborhood violence or low income has also been associated with asthma.
Though there is an influence of genetics on sensitivity to allergens, living in an urban setting
could lead to increased exposure to indoor allergens, which could lead to increased sensitization
to these allergens, promoting exacerbations of asthma. Lower SES might lead to an unhealthy
diet and to limited food selection. Unhealthy diets often lead to obesity, again associated with a
higher prevalence of asthma.
Cohen et al. claim that island Puerto Ricans suffer from asthma more than Puerto Ricans
living on the mainland U.S. (2007). Mainland Puerto Ricans have lower SES, higher rates of
premature birth, and higher rates of prenatal tobacco smoke exposure when compared to those on
the island. Yet prevalence of asthma and hospitalizations from asthma are lower for mainland
Puerto Ricans than island Puerto Ricans (Cohen et al., 2007). It is important to make the
distinction between mainland Puerto Ricans and island Puerto Ricans; often, studies will group
the two together, which could mask potential causes or triggers of asthma.
For Puerto Ricans, the association between SES and asthma is even more unclear than in
African-Americans. An association between these factors is often difficult to ascertain. Both
island and mainland Puerto Ricans often live in areas of low SES. Since little comparison can be
made between low and high SES, this would hide any impact low SES has on asthma. Since
genetics has such a large influence on asthma in Puerto Ricans, it could make the role of SES
seem insignificant.
Overall foreign-born Latinos often suffer from a lower prevalence of asthma than those
born in the U.S, possibly due to acculturation (Dumanovsky & Matte, 2007). However, this is
not true for Puerto Ricans, who have a high prevalence of asthma. Since, Puerto Ricans are
already U.S. citizens, whether they live on island Puerto Rico or the mainland U.S., they do not
28
have to go through the process of acculturation. Dumanovsky et al. explain that Puerto Ricans
are already “acculturated to dominant American institutions, practices, and habits and have the
same access to health care and social services” (2007).
Mexican-Americans struggle with the consequences of asthma just as Puerto Ricans or
African-Americans do. Because living in close proximity to other immigrants often lowers much
of the stress of moving to a new country, learning a new language, and finding a new source of
income, Cagney and Browning believe that rates of asthma are lower in immigrants living near
other immigrants (2004). Stressful situations often lead to health consequences, such as asthma.
Acculturation can lead to increased rates of asthma for Mexican-Americans (Martin et al., 2007).
With time, Mexican-Americans begin to emulate those around them, beginning to adopt the
regional belief and way of living, leading to smoking, making bad dietary decisions, increased
risk for preterm deliveries, and increasing the incidence of asthma. Country of birth and
acculturation are often cited as factors associated with asthma in Mexican-Americans, as they are
closely tied together and those born and raised in the U.S. should be more acculturated than those
born outside the U.S. U.S.-born Mexican-Americans have more exposure to the beliefs and the
living style of Americans than those born outside the U.S. Thus, it is possible that country of
birth contributes to acculturation and is not just associated with it.
In categorizing all Latinos into one group, distinctions between these minorities cannot
be made. These Latinos differ by race in prevalence of asthma, severity of asthma, and severity
of asthma exacerbations. Prevalence of asthma differs by race, even when these Latino
minorities live in close proximity to each other (Schneider, Freeman, & McGarvey, 2004). In
categorizing them into one group, it is difficult to ascertain whether conclusions derived from
research hold true for the different Latino minorities.
29
Mosnaim et al. suggest that underdiagnosis of asthma, based on parental language
preference, may lead to lower estimates of asthma in Hispanic families (2007), and found that
children whose parents preferred to answer the survey in Spanish were more likely to have
undiagnosed asthma (Mosnaim et al., 2007). Those, whose parents prefer speaking Spanish also
have better diet, are less likely to smoke, and have better outcomes because they are not yet
acculturated. This means that Mexican-born Mexican-Americans may genuinely have lower
rates of asthma than their U.S.-born counterparts.
Genetics exerts an effect on many diseases in humans, and genetic variations can lead to
a higher predisposition for asthma in certain populations. For African-Americans and Puerto
Ricans, genetics seems to lead to higher rates of asthma, more severe forms of asthma, or
lowered response to medication. It is interesting that genetics has the opposite effect on
Mexican-Americans.
Interactions between genetics and the environment likely result in asthma. This
possibility explains why people living in the same city don’t all develop asthma. For example,
though all races are likely sensitive to cockroach allergen, the level of sensitivity varies.
Cockroach allergen is highly associated with asthma in African-Americans but not in Puerto
Ricans and Mexican-Americans (Findley et al., 2003). Though they may live in the same
neighborhood and have the same level of exposure to cockroaches, genetics may determine
sensitivity.
It is difficult to determine where the effect of genetics ends and the effects of the
environment begin; it seems certain thought, that both influence asthma. Proof for the effect of
genetics can be seen in middle class African-Americans who have higher rates of asthma than
their white counterparts. The effect of the environment can also be seen with Mexican-
30
Americans born and acculturated in the United States.
31
Conclusion
Asthma is a disease of great significance and reducing the burden of asthma begins with
knowledge of the etiologies, risk factors, treatments, etc. It may be difficult to eradicate some of
the social inequalities that lead to higher rates of asthma in some minorities; however,
knowledge that these inequalities have an effect on asthma is one of the first steps in diminishing
it.
It is important to study asthma in these select minorities, since they often have a higher
frequency of asthma diagnosis or may suffer from a more severe form of asthma. Finding
answers for why one racial minority has increased rates of asthma is not easy. Sometimes, it is
purely due to noncompliance (Ortega et al., 2002). According to a study by Ortega, et al., 73%
of white asthmatics did not use inhaled corticosteroids in the past year, compared with 94% of
Hispanics (2002). Another problem arises in treating asthma in Puerto Ricans, where Burchard
et al. found that Puerto Ricans do not respond as well to albuterol, a β2-agonist, as MexicanAmericans (2004). This lack of response somewhat reduces the usefulness of albuterol. Lack of
use and ineffectiveness of these medications, which are staples of asthma treatment, have
consequences. Those, whose asthma would normally be controlled on these medications, now
suffer needlessly from asthma exacerbations, which can damage the lungs, leading to even more
severe asthma exacerbations.
Genes such as ORMDL3, DDP-10 and GPRA are associated with asthma in the general
population. However, other genes are associated with asthma in specific populations; MYLK
and KCNMB1 are associated specifically with severe asthma in African-Americans. Other
genes, such as those on regions 5p15 and 17p11.1-q11.2 are associated with asthma in AfricanAmericans, while genes on regions 2q33, 21q21, and 5q23 have been associated with asthma in
32
Hispanics (Choudhry et al., 2008; "A genome-wide search," 1997). No single gene has been
found to be responsible for asthma in white Americans, Latinos (Holberg et al., 1996), or
African-Americans. An explanation for this may be that an interaction exists between genes that
can lead to asthma. In discussing their findings from the Collaborative Study on the Genetics of
Asthma, Blumenthal et al. suggest that several regions of the human genome “may harbor genes
contributing to the risk for atopy and these may interact with one another in a complex manner”
(2004)
Herein lays a weakness of this paper and many others. It is extremely difficult to
determine how prevalent particular genes may be. While small samples of populations may
show associations between particular genes and asthma, it is difficult to determine if mutations
or variations of this gene are responsible for asthma in the entire population. Another potential
weakness of this paper is the breadth of research that has already been performed. For this
reason, search terms were kept to a minimum and studies with less than 500 asthmatic
participants were discarded, however, exceptions were made for studies which concentrated on
genetics. Since it is probably less expensive and less time consuming to analyze questionnaires
than doing genetic analysis, genetics studies often have fewer participants.
It is still not fully understood why one group has higher rates of asthma than another. In
many cases, SES is involved, either directly or indirectly. The stress of a low SES can lead to
higher rates of asthma. Low SES can lead to increased exposure to environmental agents
associated with asthma. For example, poor housing may increase exposure to asthma allergens
such as cockroaches, rodents, or molds. Housing can be in areas of poor air quality or higher
crime, leading to increased stress or fewer opportunities for outdoor activities, which can lead to
obesity. Better understanding the effect of SES on asthma could potentially help to prevent
33
asthma. By reducing the inequalities of SES, inequalities of asthma could also be reduced.
However, this is easier said than done, as these inequalities have existed for decades to centuries
in the U.S. and are not eradicated easily.
34
Future Research
An immense amount of research has already been done on asthma. One need only search
PubMed and will find monumental amounts of data. Yet, there is still much that is not known.
Future research in asthma should be aimed at one goal: to reduce the burden of asthma for those
who are most afflicted. Satcher and Rust suggest a three-dimensional model of how to reduce
disparities in lung disease, by tracking trends in prevalence, incidence, and adverse outcomes,
saying that this would give researches the ability to measure disparities at a baseline and assess
the impact of interventions on disparities (2006). They suggest researching potential causes,
cures, or interventions that may eliminate health disparities (Satcher & Rust, 2006). Though
there is significant research on causes and interventions for asthma, further research will help to
uncover other potential causes and interventions of asthma. Satcher and Rust support developing
a balanced research agenda in laboratory bench research, which would provide more information
on variables such as the pathophysiologic mechanism behind airway inflammation in asthma
(2006). A balanced research agenda is also needed with clinical trials and newer drug therapies,
and should involve the real-world primary care setting (Satcher & Rust, 2006).
Many environmental factors that affect asthma in African-Americans, such as housing
conditions, stress, and exposure to allergens, may be closely associated with socioeconomic
status. A point of future research could indicate how much effect each variable has on asthma
when it is isolated from other variables. Though, there is already some research comparing
mainland U.S. Puerto Ricans with island Puerto Ricans, future research could concentrate on
comparing the two groups to better understand some of the etiologies of asthma for Puerto
Ricans.
35
Mexican-Americans are unique among these three minorities. They have one of the
lowest rates of asthma among any minority in the U.S. Comparing asthmatics living in Mexico
with first and second generation Mexican-Americans may help in determining why new
immigrants have higher rates of asthma than their counterparts in Mexico.
For Mexican-Americans, there are large communities in California, Texas, and Illinois.
Future research should separately look at prevalence, causes, and treatment for asthma in
Mexican-Americans living in these different regions. Perhaps there are differences in the
prevalence of asthma and causes of asthma depending on the region of the U.S.
Research in African-American asthmatics could look at racial background to see
proportions of African, European, or American Indian ancestry, and try to correlate ancestry with
asthma. Also, future research could define which parts of Africa modern African-Americans
trace their ancestry. Asthmatic African-Americans could then be compared with asthmatics from
these parts of Africa. This could potentially help in determining genetic influences on asthma in
these populations.
Future research of asthma in these minorities should include the genetics of asthma.
Population-wide search for genes that are universal to all or most asthmatics of particular
minorities could help in reducing the burden of asthma. Studies of twins have been very helpful
in determining the genetic component of asthma and other related phenotypes (Los, Postmus, &
Boomsma, 2001). Many genes have been found to be associated with asthma through these
studies. Research of twins can be helpful in further discovering new genes associated with
asthma. Future research can help to determine how knowledge of the genetic component of
asthma can help in reducing rates of asthma and exacerbations of asthma (Hakonarson & Halapi,
2002).
36
Abbreviations
AIA – Aspirin induced asthma
ALA – American Lung Association
BMI – Body mass index
CDC – Centers for Disease Control
ED – Emergency Department
FEV – Forced expiratory volume
GALA – Genetics of Asthma in Latino Americans
LBW – Low birth weight
NHIS – National Health Interview Survey
RSV – Respiratory Syncytial Virus
RV - Rhinovirus
SAGE - Study of African Americans, Asthma, Genes, and Environments
37
Definitions
Albuterol – a pharmacological agent used to provide temporary relief of asthma symptoms
Hispanic – a person of Latin-American descent or Spanish descent
Latino - a person of Latin-American descent
38
References
Akinbami, L. (2006). The State of Childhood Asthma, United States, 1980–2005: CDC.
Akinbami, L. J., Rhodes, J. C., & Lara, M. (2005). Racial and ethnic differences in asthma
diagnosis among children who wheeze. Pediatrics, 115(5), 1254-1260.
American Lung Association. (2007). State of Lung Disease in Diverse Communities: 2007:
American Lung Association.
American Lung Association. (2008). Asthma. Retrieved 12/01/08, 2008, from
http://www.lungusa.org/site/apps/nlnet/content3.aspx?c=dvLUK9O0E&b=4294229&ct=
5314727
Arruda, L. K., Vailes, L. D., Platts-Mills, T. A., Fernandez-Caldas, E., Montealegre, F., Lin, K.
L., et al. (1997). Sensitization to Blomia tropicalis in patients with asthma and
identification of allergen Blo t 5. Am J Respir Crit Care Med, 155(1), 343-350.
Bai, Y., Hillemeier, M. M., & Lengerich, E. J. (2007). Racial/ethnic disparities in symptom
severity among children hospitalized with asthma. J Health Care Poor Underserved,
18(1), 54-61.
Barnes, K. C., Grant, A. V., Hansel, N. N., Gao, P., & Dunston, G. M. (2007). African
Americans with asthma: genetic insights. Proc Am Thorac Soc, 4(1), 58-68.
Beckett, W. S., Belanger, K., Gent, J. F., Holford, T. R., & Leaderer, B. P. (1996). Asthma
among Puerto Rican Hispanics: a multi-ethnic comparison study of risk factors. Am J
Respir Crit Care Med, 154(4 Pt 1), 894-899.
Berges-Gimeno, M. P., Simon, R. A., & Stevenson, D. D. (2002). The natural history and
clinical characteristics of aspirin-exacerbated respiratory disease. Ann Allergy Asthma
Immunol, 89(5), 474-478.
39
Blais, L., & Forget, A. (2008). Asthma exacerbations during the first trimester of pregnancy and
the risk of congenital malformations among asthmatic women. J Allergy Clin Immunol,
121(6), 1379-1384, 1384 e1371.
Blumenthal, M. N., Langefeld, C. D., Beaty, T. H., Bleecker, E. R., Ober, C., Lester, L., et al.
(2004). A genome-wide search for allergic response (atopy) genes in three ethnic groups:
Collaborative Study on the Genetics of Asthma. Hum Genet, 114(2), 157-164.
Boudreaux, E. D., Emond, S. D., Clark, S., & Camargo, C. A., Jr. (2003). Race/ethnicity and
asthma among children presenting to the emergency department: differences in disease
severity and management. Pediatrics, 111(5 Pt 1), e615-621.
Burchard, E. G., Avila, P. C., Nazario, S., Casal, J., Torres, A., Rodriguez-Santana, J. R., et al.
(2004). Lower bronchodilator responsiveness in Puerto Rican than in Mexican subjects
with asthma. Am J Respir Crit Care Med, 169(3), 386-392.
Burr, M. L. (1992). Diagnosing asthma by questionnaire in epidemiological surveys. Clin Exp
Allergy, 22(5), 509-510.
Cagney, K. A., & Browning, C. R. (2004). Exploring neighborhood-level variation in asthma and
other respiratory diseases: the contribution of neighborhood social context. J Gen Intern
Med, 19(3), 229-236.
Cagney, K. A., Browning, C. R., & Wallace, D. M. (2007). The Latino paradox in neighborhood
context: the case of asthma and other respiratory conditions. Am J Public Health, 97(5),
919-925.
Carroll, K. N., Griffin, M. R., Gebretsadik, T., Shintani, A., Mitchel, E., & Hartert, T. V. (2005).
Racial differences in asthma morbidity during pregnancy. Obstet Gynecol, 106(1), 66-72.
40
Choudhry, S., Taub, M., Mei, R., Rodriguez-Santana, J., Rodriguez-Cintron, W., Shriver, M. D.,
et al. (2008). Genome-wide screen for asthma in Puerto Ricans: evidence for association
with 5q23 region. Hum Genet, 123(5), 455-468.
Choudhry, S., Ung, N., Avila, P. C., Ziv, E., Nazario, S., Casal, J., et al. (2005).
Pharmacogenetic differences in response to albuterol between Puerto Ricans and
Mexicans with asthma. Am J Respir Crit Care Med, 171(6), 563-570.
Claudio, L., Stingone, J. A., & Godbold, J. (2006). Prevalence of childhood asthma in urban
communities: the impact of ethnicity and income. Ann Epidemiol, 16(5), 332-340.
Cohen, R. T., Canino, G. J., Bird, H. R., Shen, S., Rosner, B. A., & Celedon, J. C. (2007). Area
of residence, birthplace, and asthma in Puerto Rican children. Chest, 131(5), 1331-1338.
Cohen, R. T., Celedon, J. C., Hinckson, V. J., Ramsey, C. D., Wakefield, D. B., Weiss, S. T., et
al. (2006). Health-care use among Puerto Rican and African-American children with
asthma. Chest, 130(2), 463-471.
Cohen, S., Frank, E., Doyle, W. J., Skoner, D. P., Rabin, B. S., & Gwaltney, J. M., Jr. (1998).
Types of stressors that increase susceptibility to the common cold in healthy adults.
Health Psychol, 17(3), 214-223.
Coogan, P. F., Palmer, J. R., O'Connor, G. T., & Rosenberg, L. (2009). Body mass index and
asthma incidence in the Black Women's Health Study. J Allergy Clin Immunol, 123(1),
89-95.
Crump, C., Lipsky, S., & Mueller, B. A. (1999). Adverse birth outcomes among MexicanAmericans: are US-born women at greater risk than Mexico-born women? Ethn Health,
4(1-2), 29-34.
41
Davis, A. M., Kreutzer, R., Lipsett, M., King, G., & Shaikh, N. (2006). Asthma prevalence in
Hispanic and Asian American ethnic subgroups: results from the California Healthy Kids
Survey. Pediatrics, 118(2), e363-370.
Dumanovsky, T., & Matte, T. D. (2007). Variation in adult asthma prevalence in Hispanic
subpopulations in New York City. J Asthma, 44(4), 297-303.
Ehrenthal, D. B., Jurkovitz, C., Hoffman, M., Kroelinger, C., & Weintraub, W. (2007). A
population study of the contribution of medical comorbidity to the risk of prematurity in
blacks. Am J Obstet Gynecol, 197(4), 409 e401-406.
Eldeirawi, K., McConnell, R., Freels, S., & Persky, V. W. (2005). Associations of place of birth
with asthma and wheezing in Mexican American children. J Allergy Clin Immunol,
116(1), 42-48.
Erickson, S. E., Iribarren, C., Tolstykh, I. V., Blanc, P. D., & Eisner, M. D. (2007). Effect of race
on asthma management and outcomes in a large, integrated managed care organization.
Arch Intern Med, 167(17), 1846-1852.
Fauci, A. S., Braunwald, E., Kasper, D. L., Hauser, S. L., Longo, D. L., & J. Larry Jameson
Joseph Loscalzo. (2008). Harrison's: Principles of Internal Medicine (17 ed.), (pp.15961601).
Findley, S., Lawler, K., Bindra, M., Maggio, L., Penachio, M. M., & Maylahn, C. (2003).
Elevated asthma and indoor environmental exposures among Puerto Rican children of
East Harlem. J Asthma, 40(5), 557-569.
Flores, C., Ma, S. F., Maresso, K., Ober, C., & Garcia, J. G. (2007). A variant of the myosin light
chain kinase gene is associated with severe asthma in African Americans. Genet
Epidemiol, 31(4), 296-305.
42
Freeman, N. C., Schneider, D., & McGarvey, P. (2003a). Household exposure factors, asthma,
and school absenteeism in a predominantly Hispanic community. J Expo Anal Environ
Epidemiol, 13(3), 169-176.
Freeman, N. C., Schneider, D., & McGarvey, P. (2003b). The relationship of health insurance to
the diagnosis and management of asthma and respiratory problems in children in a
predominantly Hispanic urban community. Am J Public Health, 93(8), 1316-1320.
Friedman, S., & Rosenbaum, E. (2004). Nativity Status and Racial/Ethnic Differences in Access
to Quality Housing: Does Homeownership Bring Greater Parity? Housing Policy Debate,
15(4), 865-901.
Galanter, J., Choudhry, S., Eng, C., Nazario, S., Rodriguez-Santana, J. R., Casal, J., et al. (2008).
ORMDL3 gene is associated with asthma in three ethnically diverse populations. Am J
Respir Crit Care Med, 177(11), 1194-1200.
A genome-wide search for asthma susceptibility loci in ethnically diverse populations. The
Collaborative Study on the Genetics of Asthma (CSGA). (1997). Nat Genet, 15(4), 389392.
Gold, D. R., & Acevedo-Garcia, D. (2005). Immigration to the United States and acculturation as
risk factors for asthma and allergy. J Allergy Clin Immunol, 116(1), 38-41.
Goldman, L., & Ausiello, D. A. (2008). Cecil Medicine (23 ed.).
Grant, E. N., Lyttle, C. S., & Weiss, K. B. (2000). The relation of socioeconomic factors and
racial/ethnic differences in US asthma mortality. Am J Public Health, 90(12), 1923-1925.
Guendelman, S., & Abrams, B. (1995). Dietary intake among Mexican-American women:
generational differences and a comparison with white non-Hispanic women. Am J Public
Health, 85(1), 20-25.
43
Hakonarson, H., & Halapi, E. (2002). Genetic analyses in asthma: current concepts and future
directions. Am J Pharmacogenomics, 2(3), 155-166.
Hansbro, N. G., Horvat, J. C., Wark, P. A., & Hansbro, P. M. (2008). Understanding the
mechanisms of viral induced asthma: new therapeutic directions. Pharmacol Ther,
117(3), 313-353.
Haselkorn, T., Lee, J. H., Mink, D. R., & Weiss, S. T. (2008). Racial disparities in asthmarelated health outcomes in severe or difficult-to-treat asthma. Ann Allergy Asthma
Immunol, 101(3), 256-263.
Hawkins, G. A., Tantisira, K., Meyers, D. A., Ampleford, E. J., Moore, W. C., Klanderman, B.,
et al. (2006). Sequence, haplotype, and association analysis of ADRbeta2 in a multiethnic
asthma case-control study. Am J Respir Crit Care Med, 174(10), 1101-1109.
Heymann, P. W., Carper, H. T., Murphy, D. D., Platts-Mills, T. A., Patrie, J., McLaughlin, A. P.,
et al. (2004). Viral infections in relation to age, atopy, and season of admission among
children hospitalized for wheezing. J Allergy Clin Immunol, 114(2), 239-247.
Hickson, D. A., Wilhite, R. L., Petrini, M. F., White, W. B., & Burchfiel, C. (2009). Asthma and
asthma severity among African American adults in the Jackson Heart Study. J Asthma,
46(4), 421-428.
Holberg, C. J., Elston, R. C., Halonen, M., Wright, A. L., Taussig, L. M., Morgan, W. J., et al.
(1996). Segregation analysis of physician-diagnosed asthma in Hispanic and nonHispanic white families. A recessive component? Am J Respir Crit Care Med, 154(1),
144-150.
44
Holberg, C. J., Halonen, M., Wright, A. L., & Martinez, F. D. (1999). Familial aggregation and
segregation analysis of eosinophil levels. Am J Respir Crit Care Med, 160(5 Pt 1), 16041610.
Homa, D. M., Mannino, D. M., & Lara, M. (2000). Asthma mortality in U.S. Hispanics of
Mexican, Puerto Rican, and Cuban heritage, 1990-1995. Am J Respir Crit Care Med,
161(2 Pt 1), 504-509.
Hunninghake, G. M., Weiss, S. T., & Celedon, J. C. (2006). Asthma in Hispanics. Am J Respir
Crit Care Med, 173(2), 143-163.
Kang, B. (1976). Study on cockroach antigen as a probable causative agent in bronchial asthma.
J Allergy Clin Immunol, 58(3), 357-365.
Krebs, N. F., & Jacobson, M. S. (2003). Prevention of pediatric overweight and obesity.
Pediatrics, 112(2), 424-430.
Lara, M., Akinbami, L., Flores, G., & Morgenstern, H. (2006). Heterogeneity of childhood
asthma among Hispanic children: Puerto Rican children bear a disproportionate burden.
Pediatrics, 117(1), 43-53.
Li, Y. F., Tsao, Y. H., Gauderman, W. J., Conti, D. V., Avol, E., Dubeau, L., et al. (2005).
Intercellular adhesion molecule-1 and childhood asthma. Hum Genet, 117(5), 476-484.
Los, H., Postmus, P. E., & Boomsma, D. I. (2001). Asthma genetics and intermediate
phenotypes: a review from twin studies. Twin Res, 4(2), 81-93.
MacMullen, N. J., Tymkow, C., & Shen, J. J. (2006). Adverse maternal outcomes in women with
asthma: differences by race. MCN Am J Matern Child Nurs, 31(4), 263-268.
45
Martin, M. A., Shalowitz, M. U., Mijanovich, T., Clark-Kauffman, E., Perez, E., & Berry, C. A.
(2007). The effects of acculturation on asthma burden in a community sample of Mexican
American schoolchildren. Am J Public Health, 97(7), 1290-1296.
Masoli, M., Fabian, D., Holt, S., & Beasley, R. (2004). The global burden of asthma: executive
summary of the GINA Dissemination Committee report. Allergy, 59(5), 469-478.
Mastronarde, J. G., Wise, R. A., Shade, D. M., Olopade, C. O., & Scharf, S. M. (2008). Sleep
quality in asthma: results of a large prospective clinical trial. J Asthma, 45(3), 183-189.
McDaniel, M., Paxson, C., & Waldfogel, J. (2006). Racial disparities in childhood asthma in the
United States: evidence from the National Health Interview Survey, 1997 to 2003.
Pediatrics, 117(5), e868-877.
Moorman, J. E., Rudd, R. A., Johnson, C. A., King, M., Minor, P., Bailey, C., et al. (2007).
National surveillance for asthma--United States, 1980-2004. MMWR Surveill Summ,
56(8), 1-54.
Mosnaim, G. S., Sadowski, L. S., Durazo-Arvizu, R. A., Sharp, L. K., Curtis, L. M., Shalowitz,
M. U., et al. (2007). Parental language and asthma among urban Hispanic children. J
Allergy Clin Immunol, 120(5), 1160-1165.
Naqvi, M., Tcheurekdjian, H., DeBoard, J. A., Williams, L. K., Navarro, D., Castro, R. A., et al.
(2008). Inhaled corticosteroids and augmented bronchodilator responsiveness in Latino
and African American asthmatic patients. Ann Allergy Asthma Immunol, 100(6), 551-557.
Naqvi, M., Thyne, S., Choudhry, S., Tsai, H. J., Navarro, D., Castro, R. A., et al. (2007). Ethnicspecific differences in bronchodilator responsiveness among African Americans, Puerto
Ricans, and Mexicans with asthma. J Asthma, 44(8), 639-648.
46
National Heart Lung and Blood Institute. (2007). Morbidity & Mortality: 2007 Chart Book on
Cardiovascular, Lung, and Blood Diseases: National Instituation of Health: National
Heart, Lung, and Blood Institute.
Newacheck, P. W., & Halfon, N. (2000). Prevalence, impact, and trends in childhood disability
due to asthma. Arch Pediatr Adolesc Med, 154(3), 287-293.
Nicholas, S. W., Jean-Louis, B., Ortiz, B., Northridge, M., Shoemaker, K., Vaughan, R., et al.
(2005). Addressing the childhood asthma crisis in Harlem: the Harlem Children's Zone
Asthma Initiative. Am J Public Health, 95(2), 245-249.
Ogden, C. L., Flegal, K. M., Carroll, M. D., & Johnson, C. L. (2002). Prevalence and trends in
overweight among US children and adolescents, 1999-2000. JAMA, 288(14), 1728-1732.
Ortega, A. N., Gergen, P. J., Paltiel, A. D., Bauchner, H., Belanger, K. D., & Leaderer, B. P.
(2002). Impact of site of care, race, and Hispanic ethnicity on medication use for
childhood asthma. Pediatrics, 109(1), E1.
Prevalence of cigarette use among 14 racial/ethnic populations--United States, 1999-2001.
(2004). MMWR Morb Mortal Wkly Rep, 53(3), 49-52.
Roberto R. Ramirez, & G. Patricia de la Cruz. (2003). The Hispanic Population in the United
States: 2003: US Census Bureau.
Roberts, E. M. (2002). Racial and ethnic disparities in childhood asthma diagnosis: the role of
clinical findings. J Natl Med Assoc, 94(4), 215-223.
Rodriguez, M. A., Winkleby, M. A., Ahn, D., Sundquist, J., & Kraemer, H. C. (2002).
Identification of population subgroups of children and adolescents with high asthma
prevalence: findings from the Third National Health and Nutrition Examination Survey.
Arch Pediatr Adolesc Med, 156(3), 269-275.
47
Rose, D., Mannino, D. M., & Leaderer, B. P. (2006). Asthma prevalence among US adults,
1998-2000: role of Puerto Rican ethnicity and behavioral and geographic factors. Am J
Public Health, 96(5), 880-888.
Rosenbaum, E. (2008). Racial/ethnic differences in asthma prevalence: the role of housing and
neighborhood environments. J Health Soc Behav, 49(2), 131-145.
Salari, K., Choudhry, S., Tang, H., Naqvi, M., Lind, D., Avila, P. C., et al. (2005). Genetic
admixture and asthma-related phenotypes in Mexican American and Puerto Rican
asthmatics. Genet Epidemiol, 29(1), 76-86.
Sarafino, E. P., & Goldfedder, J. (1995). Genetic factors in the presence, severity, and triggers of
asthma. Arch Dis Child, 73(2), 112-116.
Satcher, D., & Rust, G. (2006). A three-dimensional approach to the elimination of racial-ethnic
disparities in lung health. Clin Chest Med, 27(3), 535-542, viii.
Schneider, D., Freeman, N. C., & McGarvey, P. (2004). Asthma and respiratory dysfunction
among urban, primarily Hispanic school children. Arch Environ Health, 59(1), 4-13.
Seibold, M. A., Wang, B., Eng, C., Kumar, G., Beckman, K. B., Sen, S., et al. (2008). An
african-specific functional polymorphism in KCNMB1 shows sex-specific association
with asthma severity. Hum Mol Genet, 17(17), 2681-2690.
Shalowitz, M. U., Sadowski, L. M., Kumar, R., Weiss, K. B., & Shannon, J. J. (2007). Asthma
burden in a citywide, diverse sample of elementary schoolchildren in Chicago. Ambul
Pediatr, 7(4), 271-277.
Smith, A. K., Lange, L. A., Ampleford, E. J., Meyers, D. A., Bleecker, E. R., & Howard, T. D.
(2008). Association of polymorphisms in CASP10 and CASP8 with FEV(1)/FVC and
48
bronchial hyperresponsiveness in ethnically diverse asthmatics. Clin Exp Allergy, 38(11),
1738-1744.
Smith, L. A., Hatcher-Ross, J. L., Wertheimer, R., & Kahn, R. S. (2005). Rethinking
race/ethnicity, income, and childhood asthma: racial/ethnic disparities concentrated
among the very poor. Public Health Rep, 120(2), 109-116.
Stevenson, L. A., Gergen, P. J., Hoover, D. R., Rosenstreich, D., Mannino, D. M., & Matte, T.
D. (2001). Sociodemographic correlates of indoor allergen sensitivity among United
States children. J Allergy Clin Immunol, 108(5), 747-752.
Stingone, J. A., & Claudio, L. (2006). Disparities in the use of urgent health care services among
asthmatic children. Ann Allergy Asthma Immunol, 97(2), 244-250.
Taranova, A. G., Maldonado, D., 3rd, Vachon, C. M., Jacobsen, E. A., Abdala-Valencia, H.,
McGarry, M. P., et al. (2008). Allergic pulmonary inflammation promotes the
recruitment of circulating tumor cells to the lung. Cancer Res, 68(20), 8582-8589.
Torres, M., Azen, S., & Varma, R. (2006). Prevalence of obesity and associated co-morbid
conditions in a population-based sample of primarily urban Mexican Americans. Ethn
Dis, 16(2), 362-369.
Trochtenberg, D. S., BeLue, R., Piphus, S., & Washington, N. (2008). Differing reports of
asthma symptoms in African Americans and Caucasians. J Asthma, 45(2), 165-170.
Tsai, H. J., Kho, J. Y., Shaikh, N., Choudhry, S., Naqvi, M., Navarro, D., et al. (2006).
Admixture-matched case-control study: a practical approach for genetic association
studies in admixed populations. Hum Genet, 118(5), 626-639.
Unger, J. B., Cruz, T. B., Rohrbach, L. A., Ribisl, K. M., Baezconde-Garbanati, L., Chen, X., et
al. (2000). English language use as a risk factor for smoking initiation among Hispanic
49
and Asian American adolescents: evidence for mediation by tobacco-related beliefs and
social norms. Health Psychol, 19(5), 403-410.
US Census Bureau. (2007). 2007 Population Estimates. from
http://factfinder.census.gov/servlet/QTTable?-ds_name=PEP_2007_EST&qr_name=PEP_2007_EST_DP1&-geo_id=01000US
US Department of Health and Human Services. (2007). National Healthcare Disparities Report:
2007.
Vargas, P. A., Simpson, P. M., Bushmiaer, M., Goel, R., Jones, C. A., Magee, J. S., et al. (2006).
Symptom profile and asthma control in school-aged children. Ann Allergy Asthma
Immunol, 96(6), 787-793.
von Mutius, E., Schwartz, J., Neas, L. M., Dockery, D., & Weiss, S. T. (2001). Relation of body
mass index to asthma and atopy in children: the National Health and Nutrition
Examination Study III. Thorax, 56(11), 835-838.
Weitzman, M., Byrd, R. S., & Auinger, P. (1999). Black and white middle class children who
have private health insurance in the United States. Pediatrics, 104(1 Pt 2), 151-157.
Wright, K. (2007). Examining racial and ethnic disparities and predictors of medication use
among California's African-American, Latino, and White children with asthma. J Natl
Black Nurses Assoc, 18(2), 1-15.
Wright, R. J., Cohen, S., Carey, V., Weiss, S. T., & Gold, D. R. (2002). Parental stress as a
predictor of wheezing in infancy: a prospective birth-cohort study. Am J Respir Crit Care
Med, 165(3), 358-365.
Wright, R. J., Finn, P., Contreras, J. P., Cohen, S., Wright, R. O., Staudenmayer, J., et al. (2004).
Chronic caregiver stress and IgE expression, allergen-induced proliferation, and cytokine
50
profiles in a birth cohort predisposed to atopy. J Allergy Clin Immunol, 113(6), 10511057.
Wright, R. J., Mitchell, H., Visness, C. M., Cohen, S., Stout, J., Evans, R., et al. (2004).
Community violence and asthma morbidity: the Inner-City Asthma Study. Am J Public
Health, 94(4), 625-632.
51
Figures
Figure 1: Asthmatics, by race, in the United States in 2001 (does not equal 100%)
Sources:
National Health Interview Service. (2001). Lifetime Asthma Population Estimates, in thousands
by Age, United States.
Figure 2: Asthma prevalence within populations in 2001
Sources:
Grieco, E. M., & Cassidy, R. C. (2001). Overview of Race and Hispanic Origin: 2000: US
Census Bureau.
Guzmán, B. (2001). The Hispanic Population: 2000: US Census Bureau.
National Health Interview Service. (2001). Lifetime Asthma Population Estimates, in thousands
by Age, United States.
52
Figure 3: Overweight, by race (females only)
Sources:
National Center for Health Statistics. (2007). Health, United States, 2007: With
Chartbook on Trends in the Health of Americans: National Center for Health
Statistics
Figure 4: This figure compares prevalence of asthma for racial groups to the national
average (computations based on data reported by the National Health Interview Service,
2001)
Source:
National Health Interview Service. (2001). Lifetime Asthma Population Estimates, in thousands
by Age, United States.
53
Figure 5: This figure compares rates of poverty, by race
Source:
Roberto R. Ramirez, & G. Patricia de la Cruz. (2003). The Hispanic Population in the
United States: 2003: US Census Bureau
U S Census Bureau. (2002). Number in Poverty and Poverty Rate by Race and
Hispanic Origin: 2001 and 2002.
Figure 6: This figure compares FEV1 response, following bronchodilator use, in those with
an FEV1 less than 80%, by race
Source:
Naqvi, M., Thyne, S., Choudhry, S., Tsai, H. J., Navarro, D., Castro, R. A., et al. (2007).
Ethnic-specific differences in bronchodilator responsiveness among African
Americans, Puerto Ricans, and Mexicans with asthma. J Asthma, 44(8), 639648.
54
Abstract
Objective: To review some of the etiologies, genetics, environmental factors, and differences in
diagnosis and/or treatment of asthma and correlate them with asthma prevalence,
hospitalizations, severity, morbidity, and mortality in African-Americans, Puerto Ricans, and
Mexican-Americans.
Method: A review of literature was performed, from 1993 through 2008, plus select sentinel
articles found through PubMed. Search terms used were: African-Americans and asthma,
asthma and Latinos, and Hispanic Americans and asthma
Results: From these search terms, 274 articles where found. Many were discarded based on
number of asthmatic participants, race of participants, year in which the study was conducted,
and subject matter of the article. Sentinel articles and reports were also included in the review.
Conclusion: Asthma is a complex disease which involves interplay of genetics and
environmental factors. Depending on race, there can be differences in diagnosis or treatment of
asthma, environmental factors that affect asthma, and influence of genetics.