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Environmental
Health Perspectives Supplements Volume 110, Number 4, August 2002
Asthma in the United States: Burden and Current Theories
Stephen C. Redd
Air Pollution and Respiratory Health Branch, National Center for Environmental
Health, Centers for Disease Control and Prevention, Atlanta, Georgia,
USA
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Full Article in PDF
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Abstract
Asthma has emerged as a major public health problem in the United States
over the past 20 years. Currently, nearly 15 million Americans have asthma,
including almost 5 million children. The number of asthma cases has more
than doubled since 1980. Approximately 5,500 persons die from asthma each
year, and rates have increased over the past 20 years. Rates of death,
hospitalization, and emergency department visits are 2-3 times higher
among African Americans than among white Americans. The costs of asthma
have also increased to $12.7 billion in 1998. Both lifestyle and environmental
hypotheses have been invoked to explain the increase in asthma prevalence.
Several studies have examined the relationship of obesity and asthma and
found associations suggesting that obesity predisposes to the development
of asthma. Some studies have found that day care attendance and having
older siblings protect against the development of asthma. This observation
has led investigators to hypothesize that increased exposure to microbial
agents might protect against asthma (the hygiene hypothesis). Environmental
exposures found to predispose to asthma include house dust mite allergen
and environmental tobacco smoke. Although current knowledge does not permit
definitive conclusions about the causes of asthma onset, better adherence
to current recommendations for medical therapy and environmental management
of asthma would reduce the burden of this disease. Key words: asthma,
epidemiology, hygiene, incidence, indoor environment, obesity. Environ
Health Perspect 110(suppl 4):557-560 (2002).
http://ehpnet1.niehs.nih.gov/docs/2002/suppl-4/557-560redd/abstract.html
This article is part of the monograph Environmental
Air Toxics: Role in Asthma Occurrence?
Address correspondence to S.C. Redd, CDC, 6 Executive
Park Dr., Bldg. 6, Room 1019, Atlanta, GA 30329 USA. Telephone: (404)
498-1019. Fax: (404) 498-1088. E-mail: scr1@cdc.gov
Received 27 November 2001; accepted 27 February 2002.
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Epidemiology and Economic Impact of Asthma
Asthma has emerged as a major public health problem in the United States over
the past 20 years. This overview of the epidemiology of asthma in the United
States a) reviews what we know about asthma in the United States, including
its cost; b) describes several current theories that might explain the
phenomenon we are experiencing; and c) discusses what we should be doing
to control this modern epidemic of a chronic and environmental disease.
The striking fact is that asthma is much more common than it was 20 years ago.
The number of persons with self-reported asthma has more than doubled between
1980 and 1996 (Figure 1), with the greatest increase in the prevalence rate
among children of preschool age (1). Although the diagnosis of asthma
is more difficult among young children (and potentially confounded by comorbid
conditions in older persons), the magnitude of the increase suggests that it
is not due solely to changes in diagnostic practices or changes in coding practices.
Work from Olmstead County, Minnesota, documented an increasing asthma incidence
rate from 1964 to 1983 among children (2). National data show increases
in prevalence in all age, race, and ethnic groups and among both males and females.
Data from a recent survey that collected information only on adults suggest
that this trend has continued; the estimated number of adults with asthma has
reached 14.6 million persons, 7.2% of the U.S. population (3).
 |
| Figure 1. Number of people with asthma, United States,
1980-1996. |
As the number of cases of asthma was increasing, so was the number of persons
dying from asthma (Figure 2) (1). Most deaths due to asthma occurred
in adults over 35 years of age, especially among adults over 65 years of age.
This increase dates from the mid-1970s, when deaths from asthma reached a nadir.
The rate of hospitalization for asthma increased during the late 1980s and has
since plateaued. However, the rate among African Americans remained 2-3 times
higher than for white Americans (Figure 3). Similar disparate outcomes also
exist between white American and African Americans for the rates of death and
of emergency department visits. Hispanic Americans in the Northeast also have
an elevated risk for death compared with white Americans (4).
This disparity in outcomes defines one of the key research themes that must
be addressed to improve the national picture for asthma.
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Figure 2. Deaths due to asthma, United States,
1960-1995.
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In addition to better understanding disparities among different race and ethnic
groups, we need better surveillance data, specifically data that are more timely
and geographically appropriate. Such data will facilitate planning and evaluation
of local interventions. With the exception of mortality data and data from the
Behavioral Risk Factor Surveillance System (3), data are available at
regional or national levels only. In addition prevalence rates in the published
literature vary widely. It is generally not possible to determine the reasons
for this range, although a number of definitions of asthma have been used (including
having the symptoms of asthma rather than having physician-diagnosed asthma
and ever having been diagnosed with asthma as opposed to currently having asthma),
and surveys have been conducted of specific populations at higher risk for asthma
than the general population. Surveillance for incident cases of asthma is needed
for investigators to better understand why prevalence is increasing. Identifying
the characteristics of incident cases would also facilitate studies of the risk
factors for the onset of asthma.
The economic costs of asthma to the nation are substantial. Weiss et al. estimated
the direct and indirect costs to be $6.2 billion during 1990 (5). In
2000, these estimates were updated and different sources of cost were compared
with those from the earlier period (6). Overall, costs increased approximately
50%. Hospital and emergency department costs had declined and costs for pharmaceuticals
had increased. This report (6) examined differences in prescribing patterns
in the two time periods found that short-acting beta agonists--rescue medications
used for the immediate relief of symptoms--had increased to a much greater extent
than had the anti-inflammatory agents--medications used to prevent symptoms
in persons with persistent asthma. Data from these studies indicated that the
estimated cost of asthma rose slightly from 1.16% of direct medical expenses
in 1985 to 1.48% in 1994.
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Figure 3. Rate of hospitalization
due to asthma, United States, 1980-1998.
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Theories on the Origins of the Asthma Epidemic
Asthma has emerged as a substantial problem in the United States. Inexpensive,
easy-to-implement interventions to prevent the onset of asthma have not been
defined despite some research on the effectiveness of allergen avoidance measures
(7,8). In fact despite a substantial research effort, the exact causes
of nonoccupational asthma are poorly defined. Such definition is a vital prerequisite
to establishing and implementing public health approaches to prevent asthma
onset. Currently, investigators have proposed several theories to explain the
increase in asthma prevalance. Below, I briefly review research that points
to two lifestyle or behavioral risk factors. I then provide an overview of a
review of the role that indoor exposures may play in contributing to the asthma
epidemic.
Potential Lifestyle or Behavioral Risk Factors for Asthma for Asthma Onset
The first hypothesis to explain the increasing prevalence of asthma begins
with the observation that an increasing proportion of the U.S. population is
overweight or obese and that this trend parallels the increasing prevalence
rate of asthma (9). Several investigators suggest that these similarly
increasing trends are more than coincidental, and some evidence has been collected
to suggest a relationship between obesity and reduced lung function or asthma
(10-12). In one of the first prospective studies, Camargo et al.
(10) examined data from the Nurses' Health Study. Incident asthma was
identified from among 85,911 adult female nurses over a 4-year period. Follow-up
questionnaires were sent to individuals who may have had new-onset asthma during
the observation period to collect additional information on the details of the
onset of disease. Three levels of certainty of new-onset asthma were constructed
and examined as the outcomes for a variety of risk factors, including body mass
index (calculated as weight in kilograms divided by height in meters squared--all
collected by questionnaire). A total of 1,596 new-onset asthma cases were identified,
an annual incidence rate of 0.5%. The authors found a dose-response effect
for body mass indices above 20, with progressively greater risk for new-onset
asthma with increasing body mass index. In addition, the risk was progressively
greater for each level of specificity of the case definition of new-onset asthma,
with the strictest definition having the greatest risk. The authors also had
information on physical activity and found similar trends for increasing risk
of asthma with decreasing levels of physical activity. Further study is needed
to verify these findings in other populations, including men and children, and
to determine the effectiveness of weight loss as an intervention to reduce the
risk of developing asthma.
The second hypothesis has become known popularly as the "hygiene hypothesis."
Several studies have shown that having older or a greater number of siblings
protects a child from developing asthma (13,14). This protection against
developing asthma might be, in part, the result of exposure to infections acquired
from older siblings. The study that I describe here in more detail was conducted
in Tucson, Arizona (15), and examined the risk for developing asthma
in a cohort of children born between 1980 and 1984. Information about the onset
of asthma and about two cardinal symptoms of asthma--wheezing and whistling
in the chest--was collected with a standard questionnaire. Risk factors for
asthma onset included the number of older siblings and their ages at the time
of enrollment in day care. Children with older siblings were at lower risk for
asthma at 11 and 13 years of age. Enrollment of infants 0-4 months of age
in day care likewise was associated with a reduced risk of asthma at 11 and
13 years of age compared with enrollment at older ages or not attending day
care. Asthma symptoms at 2 years of age were more likely among children with
older siblings or early attendance in day care but less likely at 11 and 13
years of age.
These results suggest that asthmalike symptoms in early childhood could be
caused by infection; experience with infection early in life could then result
in reduced subsequent risk for allergic asthma (16). This immunological
explanation has some basis in what is known about the development of the immune
system in early life. The T-helper (TH) cell line of lymphocytes
has two distinct components: TH1, which mediates cell-mediated immunity
and is a mature manifestation of immune function, and TH2, which
mediates antibody production (16). At the time of birth, TH
lymphocytes are largely TH2; over time a TH1 type of immune
response develops. According to the hygiene hypothesis, modern life with reduced
risk of infection is associated with a skewing of the population toward TH2-type
immune responses. TH1 and TH2 are defined in a practical
sense by measuring the production of various cytokines, with specific cytokines
being associated with TH1 or TH2 immune responses. These
data do not yet provide a definitive conclusion on whether improved hygiene
has caused the increase in asthma prevalence (17,18).
Environmental Exposures and Asthma Onset
In addition to the overweight/physical activity hypothesis and the hygiene
hypothesis, many investigators have sought to identify specific environmental
exposures associated with the development of asthma. With the exception of specific
work-related exposures (19), this effort has not produced a unifying
theory or set of observations to explain the asthma epidemic. The U.S. Environmental
Protection Agency commissioned the Institute of Medicine to review the available
evidence for relationships between indoor environmental exposures and asthma
to make recommendations for mitigating these exposures on the basis of the scientific
literature and to suggest areas for future research. In 2000, the Institute
of Medicine published a report based on this review. The review is comprehensive
and is concerned with both exposures that may be related to onset of asthma
and factors related to worsening of already established asthma (20).
An elaborate classification scheme was used to evaluate each exposure; the evidence
was categorized as follows: a) exposures with evidence of a causal relationship,
b) exposures with evidence of an association, c) exposures with
limited or suggestive evidence, d) exposures with inadequate evidence,
and e) exposures with limited or suggestive evidence of no association.
For biological exposures related to the development of asthma, exposure to
house dust mite allergen was classified as having evidence of a causal relationship.
Exposure to cockroach allergen and exposure to respiratory syncytial virus were
classified as having limited or suggestive evidence. Exposure to rhinovirus
among adults was classified as having limited or suggestive evidence of no association.
Inadequate or insufficient evidence was found of an association of exposure
of mold and asthma onset. For chemical exposures, exposure to environmental
tobacco smoke among children of preschool age had evidence of an association.
All other exposures were classified as having inadequate evidence.
This lengthy review (20), from which only the conclusions have been
cited, also included suggestions for future research. The committe at the Institute
of Medicine recommended an emphasis on examining exposures early in life, including
prenatal exposures, and on attempting to define the age at first exposure to
substances that could be related to the onset of asthma. The committee stressed
the need for improved understanding of gene-environment interactions. In
addition, the committee suggested the need to examine exposure reduction strategies
and to include rigorous mitigation trials. Ultimately, better integration of
the health sciences and healthy environment sciences is needed to achieve these
research aims.
Up to this point I have concentrated on indoor environmental exposures. Ambient
or outdoor environmental exposures to ozone and particulate matter (as well
as sulfur dioxide and nitrogen oxides) are well-documented causes of asthma
exacerbations (21). Data on emergency department visits, hospitalizations,
and symptoms have shown clear associations with both of these pollutants (21,22).
What is much less clear is whether ambient outdoor pollution is associated with
asthma onset. At a gross level, air pollution levels are lower than they were
in the past, yet asthma prevalence has risen substantially over the past 20
years (23). This conclusion ignores the differences in changes in air
pollution: a sharp reduction for ambient lead but hardly any change in ozone
levels. It also overlooks the lack of information on asthma onset and the paucity
of studies that have examined exposure to specific pollutants as risk factors
for asthma onset. It is likely that such information will be available within
the next several years. One study that will have the ability to assess such
associations is being conducted in 12 southern California communities (24).
A recent analysis showed that children who played three team sports and lived
in communities with higher ambient ozone concentrations were at increased risk
for developing asthma compared with children who lived in communities with lower
ozone concentrations or who played fewer team sports (25). Although this
report should not be interpreted as the final word on the risk of outdoor air
pollution for asthma onset, it does demonstrate the type of analysis needed
to assess the risk of ambient outdoor exposures for asthma onset.
Summary and Conclusions
In this brief review of asthma epidemiology in the United States, I have highlighted
trends in the increasing number of cases, increases in the number of deaths,
and the racial and ethnic disparities in the more severe outcomes of asthma.
Several theories have been proposed to explain the increased number of cases,
but evidence is inadequate to fully explain the phenomenon that has occurred
in the United States over the past 20 years. Two indoor environmental exposures--exposure
to house dust mites and to environmental tobacco smoke among children of preschool
age--have been shown to cause or be associated with asthma onset. Although outdoor
ambient environmental exposures are known to cause asthma exacerbations, very
limited evidence is available to suggest that these exposures can actually cause
the disease itself. Future work may provide more definitive conclusions.
Public health efforts need to be based on current knowledge. Established guidelines
for the environmental and medical management of asthma (26) are not being
followed (27,28). If they were followed, a substantial reduction in morbidity
and mortality would be expected. Improved implementation of these consensus
guidelines as well as intensified efforts to track the prevalence, severity,
and quality of asthma management is needed to reduce the needless burden of
asthma.
References and Notes
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Last Updated: August 6, 2002
