Environmental Health Perspectives Volume
103, Supplement 6, September 1995
[Citation
in PubMed]
Environmental Risk Factors of Childhood Asthma in Urban Centers
Floyd J. Malveaux and Sheryl A. Fletcher-Vincent
Departments of Microbiology and Medicine, Howard University College of
Medicine, Washington, DC.
Abstract
Asthma morbidity and mortality are disproportionately high in urban centers,
and minority children are especially vulnerable. Factors that contribute
to this dilemma include inadequate preventive medical care for asthma management,
inadequate asthma knowledge and management skills among children and their
families, psychosocial factors, and environmental exposure to allergens
or irritants. Living in substandard housing often constitutes excess exposure
to indoor allergens and pollutants. Allergens associated with dust mites
(DM) and cockroaches (CR) are probably important in both onset and worsening
of asthma symptoms for children who are chronically exposed to these agents.
Young children spend a great deal of time on or near the floor where these
allergens are concentrated in dust. Of children (2-10 years of age) living
in metropolitan Washington, DC, 60% were found to be sensitive to CR and
72% were allergic to DM. Exposure to tobacco smoke contributes to onset
of asthma earlier in life and is a risk factor for asthma morbidity. Since
disparity of asthma mortality and morbidity among minority children in urban
centers is closely linked to socioeconomic status and poverty, measures
to reduce exposure to environmental allergens and irritants and to eliminate
barriers to access to health care are likely to have a major positive impact.
Interventions for children in urban centers must focus on prevention of
asthma symptoms and promotion of wellness. -- Environ Health Perspect
103(Suppl 6):59-62 (1995)
Key words: asthma, indoor environment, urban centers, indoor allergens,
cockroach allergens, dust mite allergens
This article was presented at the symposium on Preventing
Child Exposures to Environmental Hazards: Research and Policy Issues held
in Washington, DC, 18-19 March 1993.
The research was supported in part by a grant from Hasbro
Children's Foundation, New York.
Address correspondence to Dr. Floyd J. Malveaux, Department
of Microbiology, Howard University College of Medicine, 520 W Street, NW,
Washington, DC 20059. Telephone (202) 806-6284. Fax (202) 806-4508.
Introduction
Asthma morbidity and mortality are disproportionately high among African
American (AA) children who live in urban areas, especially those of relatively
low socioeconomic status (SES). Inadequate preventive medical care for asthma
management and lack of asthma knowledge and management skills among children
and their families are significant contributing factors to this problem.
Asthma mortality is 5 to 7 times higher for AA children than their white
counterparts (1) and they are twice as likely to be hospitalized
for asthma (2). Recent studies suggest that the disparity of mortality
and morbidity are closely associated with SES, and that poverty rather than
race or ethnicity is a more significant risk factor (2,3). AA children
have a 20% higher prevalence of asthma than Caucasian children.
There are a number of studies that clearly demonstrate that asthma mortality
and morbidity are worse in urban centers than elsewhere. For example, in
Cook County, Illinois, a disproportionately high percent of asthma deaths
occurred in the inner city (4) and in East Harlem the rate was 10
times that of the average rate in the United States (5). Hospitalization
rates for asthma show a similar pattern. Between 1982 and 1986 hospitalizations
for asthma in different neighborhoods of New York City showed the highest
rate (115/10,000 population) to be in East Harlem and was 16 times higher
than that of the lowest rate (7.2/10,000), which occurred in Greenwich Village-Soho
in Manhattan (5). In Maryland, excess hospitalization rates were
noted in children living in the inner city (2).
Disparity of asthma morbidity that exists in urban centers reflects
to a great degree the gap that exists in SES and accessibility of health
care (especially preventive care) in patients of relatively low SES. For
example, 50% of African American and 42% of Hispanic children are poor (6),
and regular health care (whenever present) for the poor is more likely to
be in an emergency room (ER) (7). Insurance status is often a strong
predictor of access to care in low income populations (8). Case-controlled
studies have identified some risk factors that are associated with increased
asthma mortality and morbidity: hospitalization(s) in the recent past; frequent
ER visits; previous life-threatening episodes of asthma; inadequate or delayed
treatment of acute attacks; labile or deteriorating lung function; cultural
or economic barriers to health care (9). Other risk factors are associated
with problems that are characteristic of poverty and the urban center, and
day to day life stresses pose barriers to seeking regular and preventive
care.
In some cases asthma of children living in urban centers is very difficult
to manage. This may due to intrinsic or extrinsic factors. An example of
intrinsic factors may be abnormal lung development and function (e.g., premature
birth). Extrinsic factors may include the result of chronic exposure to
allergens or irritants or psychosocial problems. Many children in urban
centers live in substandard housing where exposure to indoor allergens and
pollutants (especially tobacco smoke) constitutes a risk factor that can
be controlled to a limited degree. In urban dwellings, allergens associated
with dust mites (DM) and cockroaches (CR) are believed to be important in
both onset and worsening of asthma symptoms. For example, it has been shown
that exposure to high levels of mite allergen (in dust) during infancy or
in the first year of life results in the increased likelihood of sensitization
and positive skin tests to these allergens and the development of asthma
(below). Conversely, when mite allergen levels are significantly reduced
in the home, the frequency of asthma symptoms is reduced.
One of the earliest reports suggesting a role for CR in asthma was that
of a study 30 years ago by Bernton and Brown (10). In a recent survey
in our clinics at Howard University Hospital in Washington, DC 60% of children
(2-10 years of age) were positive to CR (11). This rate of sensitization
to CR was comparable to that (58%) found in an atopic population in Chicago
where bronchial challenges were also done (12). Reductions in pulmonary
function following challenge with CR were noted and strongly suggested a
causative role of CR in asthma symptoms in this urban population.
Of urban subjects with asthma and positive skin reactivity to CR antigen,
91% had immediate positive bronchial reactivity, and 48% had late-phase
reactions (13). The prevalence of CR allergy among asthma patients
is directly related to socioeconomic status and CR allergy in asthmatics
of low SES is common, ranging from 52 to 78% (11). The potential
importance of CR asthma is underscored by the postulation that recurrent
exposure to allergens may be responsible for the airway inflammation
in asthma (14).
In general, children with asthma who are exposed to passive tobacco smoke
(TS) have been shown to have increased emergency room visits, impaired lung
function, and a higher requirement for medications. There is evidence that
there is a dose response between the number of cigarettes smoked and the
length of time of smoking with the severity of asthma symptoms in children.
Exposure to TS contributes to onset of asthma earlier in life and is a risk
factor for frequent ER visits.
The health effects of environmental tobacco smoke are being increasingly
identified and the effect of environmental TS on respiratory function and
lung disease in children has been a particularly intense area of investigation.
Tobacco smoke is ubiquitous in the workplace, public and private establishments,
and in the home, making exposure to environmental TS virtually unavoidable.
In a study of nonsmokers and former smokers, 63.3% of nonsmokers reported
some daily exposure, 34.5% reported exposure of at least 10 hours per week
and 15.9% reported at least 40 hours of exposure per week (15). About
70% of children in the United States live in homes where there is at least
one adult smoker (16).
There is a consistently observed effect of environmental TS from parental
smoking on a number of acute childhood respiratory illnesses. Infants of
smoking mothers have a greater number of hospital admissions for pneumonia
and bronchitis than children of nonsmoking parents (17), and are
more likely to have pneumonia and bronchitis during the first year of life
(18). There is an increased frequency of tracheitis and bronchitis
in infants whose parents smoked, most of the risk is derived from maternal
smoking (19).
A study of random community-based populations in Michigan and Massachusetts
showed that children of smokers were more likely to have asthma, particularly
severe asthma, than children of nonsmoking parents (20). In a study
of children aged 7 to 17 years with a history of asthma, the children of
mothers who smoked had 47% more symptoms, a lower FEV1 (13% lower), and
a fourfold greater responsiveness to a histamine challenge test than asthmatic
children of nonsmoking mothers (21). Additionally, a study of asthmatic
children showed a significant increase of 63% in asthma-related visits to
an ER by children exposed to parental tobacco smoke (22). The published
data to date suggest that parental smoking, particularly maternal smoking,
increases the frequency and severity of asthmatic attacks (23).
Interventions in the Inner City
Too few interventions have been tried in patients in urban centers. The
long-term effectiveness of education in modifying behavior is unknown; but
it is likely that education alone of patients and their families, especially
about the importance of preventive care, will significantly reduce mortality
and morbidity. Measures to reduce exposure to environmental allergens and
irritants and to eliminate some of the barriers to access to health care
are likely to make a major positive impact.
The roles of education and avoidance of allergens and irritants cannot
be overemphasized. Children with asthma have hyperresponsive airways, and
the need to understand the chronicity of this disease will avoid the episodic
approach to both nonpharmacologic and pharmacologic management. Education
involves helping families understand asthma and learn and practice skills
necessary to manage the illness. Providing information (written or verbal)
is necessary, but is not sufficient to accomplish these objectives. Education
must begin at the time of diagnosis and continue with each office visit
and telephone call. Each office visit, however brief, should be viewed as
an opportunity for patient and family education. The educational needs of
patients and families may change with time and should be assessed at regular
intervals. Encouraging active participation in a partnership with the clinician
will improve environmental control measures and patient adherence to a management
plan.
Avoidance of allergens and irritants that produce airway narrowing is
important since these factors are known to provoke acute symptoms and increase
airway hyperresponsiveness. This, in turn, increases vulnerability to further
irritant and allergen exposure. If allergy plays a role in a patient's asthma
symptoms, environmental control measures to avoid specific allergens are
of paramount importance, and immunotherapy may be indicated in selected
patients.
Central to the health effects of indoor allergens and the importance
of education is the role of allergen avoidance as a primary method of promoting
good health and controlling diseases initiated or exacerbated by exposure
to these allergens. For example, mite allergen avoidance is considered an
important method of treatment for dust mite allergy (24) and is also
associated with improvement of asthma when rigorous methods of avoidance
are employed (25). In the Canadian study by Murray and Ferguson there
were substantial reduction in bronchial hyperreactivity and medication requirements
in ten children who used mite avoidance measures. The regimen was stringent
and included removing carpets, sealing heating ducts, and removing from
the home animals to which the children had positive allergy skin tests (26).
Studies suggest that allergen avoidance reduces morbidity of asthma in
sensitized individuals and that there is correlation of high prevalence
of immediate hypersensitivity to common indoor allergens and existence of
threshold levels of exposure in individuals at risk. Recent progress in
the immunochemical detection of common indoor allergens such as cat, dust
mite, and cockroaches makes it possible to measure exposure to these allergens
and to define the threshold levels of exposure that are needed to effect
sensitization and increased symptoms (27). For example, it has been
suggested that exposure to greater than 2 µg group I dust mite allergen
(or 100 mites) per gram of dust increases the risk of children's developing
sensitization and asthma. In addition to the risk of sensitization to allergens
derived from cats, cockroaches, and grass pollen, endotoxins are strongly
suspected as potent pro-inflammatory substances in individuals exposed
to high levels of these allergens (28). Finally, in a prospective
study in a cohort of British children at risk of allergic disease because
of family history, there was a trend toward sensitization to dust mites
by age 11 when exposure to antigen at age 1 had been to more than 10 µg
Der p I/g of dust (29). The age at which wheezing first occurred
was positively related to the level of exposure at age 1 for all children,
but especially for those who had a family history of atopy. In this study
it is suggested that in addition to genetic factors, exposure to certain
allergens in early childhood may be a an important determinant for subsequent
development of respiratory diseases such as asthma. Thus, avoidance of indoor
allergens may be important in managing asthma and will likely be significant
in reducing morbidity in susceptible individuals.
Future studies are necessary to answer the questions of how stringent
and for how long avoidance measures should be attempted, since not all studies
have been uniformly positive in demonstrating the beneficial effect of allergen
avoidance on allergic diseases (30). Among 26 children with mild
to moderate asthma who participated in a controlled trial of dust mite avoidance
for up to 12 weeks, there was no significant difference among the study
and control groups in bronchial reactivity to histamine, symptom scores,
peak expiratory flow rates, or medication requirements. However, the
measures of avoidance were less stringent than those of the studies cited
above. On the other hand, it is argued that it may be difficult to convince
parents of children with mild to moderate asthma (as opposed to severe asthma)
that more stringent methods are warranted. While this study failed to show
clinical benefit from mite avoidance, there was a fall in total serum IgE,
the significance of which is unknown at present. The long-term effects of
avoidance and the appropriate patient population on whom such measures may
be effective are presently unknown.
In some cases objective monitoring of lung function may be an important
means of monitoring exposure to allergens and irritants. Peak Expiratory
Flow Rates (PEFR) have been reported to be useful in daily monitoring to
detect early stages of airway obstruction and as a guide to initiate therapy;
in determining when emergency care is needed; and in obtaining daily measures
to investigate the potential role of allergens at home or in the workplace.
Further studies are needed to determine which group of patients (e.g., by
severity of asthma) or under what circumstances monitoring of PEFR will
be effective.
Summary
Studies to date suggest that indoor allergens and irritants play a significant
role in level of asthma morbidity experience by children living in urban
centers. Although relatively few controlled studies have been done to assess
the significance of and to intervene in reducing exposure to environmental
allergens (especially indoor allergens) and irritants in this population,
the following suggestions can be made:
* provide education to patients and health care providers about
environmental risk factors (allergens and irritants), especially in urban
centers;
* stress prevention of asthma symptoms and promote days of wellness
and normal function;
* initiate and maintain surveillance of individuals and groups
who are at risk of exposure to high levels of allergens and irritants.
REFERENCES
1. Malveaux FJ. Deaths from asthma by race, sex, and age.
1979-83. J Allergy Clin Immunol 79:183 (1987).
2. Wissow L, Gittelsohn A, Szklo M, Starfield B, Mussman
M. Poverty, race, and hospitalization for childhood asthma. Am J Public
Health 78:777-782 (1988).
3. Halfon N, Newacheck PW. Childhood asthma and poverty:
differential impacts and utilization of health services. Pediatrics 91:59-61
(1993).
4. Marder D, Targonsky P, Orris O, Persky V, Addington
W. Effect of racial and socioeconomic factors on asthma mortality in Chicago.
Chest 101:427S-430S (1992).
5. Carr W, Zeitel L, Weiss K. Asthma hospitalization and
mortality in New York City. Am J Public Health 82:59-65 (1992).
6. Data Sourcebook: Five Million Children. New York: Columbia
University National Center for Children in Poverty 1990;9.
7. Neighbors HW. Ambulatory medical care among adult Black
Americans: the hospital emergency room. J Natl Med Assn 78:275-282 (1986).
8. Hubbell F, Waitzkin H, Mishra S, Dombrink J. Evaluating
health care needs of the poor: a community-oriented approach. Am J Med 87:127-131
(1989).
9. Rea HH, Scragg R, Jackson R, Beaglehole R, Fenwick J,
Sutherland, DC. A case-controlled study of deaths from asthma. Thorax 41:833-839
(1986).
10. Bernton H, Brown H. Insect allergy: preliminary studies
of the cockroach. J Allergy 35:6 (1964).
11. Fletcher-Vincent S, Reece ER, Malveaux FJ. Reactivity
to cockroach and other allergens in an inner city population with rhinitis
and asthma. J Allergy Clin Immunol 93:174 (1994).
12. Kang B. Study on cockroach antigen as probable causative
agent in bronchial asthma. J Allergy Clin Immunol 58:357-365 (1976).
13. Kang B, Vellody D, Homburger H, Yunginger JW. Cockroach
cause of allergic asthma: its specificity and immunologic profile. J Allergy
Clin Immunol 63:80-86 (1979).
14. Cockcroft D. Lancet 1:253 (1983).
15. Friedman GD, Pettiti DB, Bawol RD. Prevalence and correlates
of passive smoking. Am J Public Health 73:401-405 (1983).
16. Weiss ST. Passive smoking and lung cancer: what is
the risk? Am Rev Respir Dis 133:1-3 (1986).
17. Harlap S, Davies AM. Infant admissions to hospital
and maternal smoking. Lancet 1:529-532 (1974).
18. Colley JR, Holland WW, Corkhill RT. Influence
of passive smoking and parental phlegm on pneumonia and bronchitis in early
childhood. Lancet 2:1031-1034 (1974).
19. Pedreira FA, Guandolo VL, Ferali EJ, Mella GW, Weiss
LP. Involuntary smoking and incidence of respiratory illness during the
first year of life. Pediatrics 75:594-597 (1985).
20. Gortmaker SL, Walker DK, Jacobs FH, Ruck-Ross H. Parental
smoking and the risk of childhood asthma. Am J Public Health 72(6):574-579
(1982).
21. Murray AB, Morrison BJ. The effect of cigarette smoke
from the mother on bronchial responsiveness and severity of symptoms in
children with asthma. J Allergy Clin Immunol 77(4):575-581 (1986).
22. Evans D, Levison MJ, Feldman H, Clark NM, Wasilewski
Y, Levin B, Mellins RB. The impact of passive smoking on emergency room
visits of urban children with asthma. Am Rev Respir Dis 135:567-572 (1987).
23. Fielding JE, Phenow RJ. Health effects of involuntary
smoking. N Engl J Med 319:1452-1460 (1988).
24. Buckley JM, Pearlman DS. Controlling the environment
for allergic diseases. In: Allergic Diseases from Infancy to Adulthood,
2nd ed, (Bierman CW, Pearlman DS, eds). Philadelphia:W.B. Saunders Company,
1989;239-252.
25. Platts-Mills T, Tovey EB, Mitchell EB, Moszoro H, Nock
P, Wilkins SR. Reduction of bronchial hyperreactivity during prolonged allergen
avoidance. Lancet 2:675-678 (1982).
26. Murray AB, Ferguson AC. Dust-free bedrooms in the treatment
of asthmatic children with house dust or house dust mite allergy: a controlled
trial. Pediatrics 71:418-422 (1983).
27. Platts-Mills T, Ward GW, Sporik R, Gelber L, Chapman
MD, Heymann P. Epidemiology of the relationship between exposure to indoor
allergens and asthma. Int Arch Allergy Appl Immunol 94:339-345 (1991).
28. Michel O, Ginanni R, Duchateau J, Vertongen F, Le Bon
B, Sergysels R. Domestic endotoxin exposure and clinical severity of asthma.
Clin Exp Allergy 21:441-448 (1991).
29. Sporik R, Holgate ST, Platts-Mills T, Cogswell J. Exposure
to house dust mite allergen (Der p I) and the development of asthma in childhood:
a prospective study. N Engl J Med 323:502-507 (1990).
30. Gillies DRN, Littlewood JM, Sarsfield JK. Controlled
trial of house dust mite avoidance in children with mild to moderate asthma.
Clin Allergy 17:105-111 (1987).
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