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Parent-Reported Environmental Exposures and Environmental Control Measures for Children With Asthma
Jonathan A. Finkelstein, MD, MPH;
Anne Fuhlbrigge, MD, MS;
Paula Lozano, MD, MPH;
Evalyn N. Grant, MD;
Reeva Shulruff, MD;
Kelly E. Arduino, MA;
Kevin B. Weiss, MD, MPH
Arch Pediatr Adolesc Med. 2002;156:258-264.
ABSTRACT
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Background Mounting evidence suggests that indoor allergens and irritants contribute
to childhood asthma. National asthma guidelines highlight the importance of
their reduction as part of comprehensive asthma treatment.
Objectives To assess the prevalence of potential environmental triggers, to identify
risk factors for such exposures, and to determine whether prior parental education
about trigger avoidance is associated with fewer such exposures.
Setting and Patients Children with asthma in practices affiliated with 3 managed care organizations.
Interventions Parents of 638 children, aged 3 to 15 years, were interviewed on enrollment
in a randomized trial of asthma care improvement strategies. Parents reported
recent asthma symptoms and exposures to potential environmental triggers.
Multivariate models were used to identify specific demographic risk factors
for environmental exposures and to determine if prior education was associated
with fewer such exposures.
Results Exposures to environmental triggers were frequent: 30% of households
had a smoker, 18% had household pests, and 59% had furry pets. Other exposures
included bedroom carpeting (78%) and forced-air heat (58%). Most children
did not have mattress (65%) or pillow (84%) covers. Of the parents, 45% reported
ever receiving written instructions regarding trigger avoidance and 11% reported
them given in the past year. However, 42% reported discussing triggers in
the home environment with a clinician in the past 6 months. In multivariate
models, predictors of smoking at home included low annual family income and
lower parental educational attainment. Dog ownership was associated with low
educational attainment, and dog and cat ownership were less likely with black
race. Reports of pests were increased for black children compared with white
children. Black race was associated with lower rates of other exposures, including
bedroom carpeting. After controlling for potential confounders, there was
no association of reduced exposures with prior receipt of environmental control
instructions.
Conclusions Exposure to potential environmental triggers is common, and recommended
trigger avoidance measures are infrequently adopted. While specific exposures
may vary with demographic and socioeconomic variables, all children are at
risk. New methods for educating parents to reduce such exposures should be
tested.
INTRODUCTION
THE INCREASE in childhood asthma prevalence and morbidity during the
past 2 decades has been substantial, with the highest rates reported among
poor, urban, and minority populations.1-2
Mounting evidence points to exposure to indoor allergens and irritants, sometimes
associated with poor housing conditions, as a major contributor to childhood
asthma.3-5 Exposure
to environmental tobacco smoke has consistently been shown to increase asthma
risk for children.6-9
Studies have implicated dust mites,10 cockroaches,11-12 mice and cats,13
and other furry pets as contributing to asthma morbidity. Exposures to mice
and cockroaches have been shown to be especially common in asthmatic patients
living in inner-city housing.11, 14
Positive skin test results to specific allergens, including dog, cat, and
indoor molds, have been associated with sensitivity to inhaled methacholine
chloride.15 A review5
by the US Institute of Medicine recently found evidence of a causal relationship
between exacerbations and dust mite, cockroach, and cat exposure in sensitized
individuals and sufficient evidence of an association between exacerbations
and exposure to dogs and fungi (molds).
National and international guidelines for the treatment of asthma, disseminated
since 1991,16-18
highlight the importance of the reduction of environmental triggers as part
of a comprehensive approach to asthma treatment. However, Lanphear et al19 recently reported that 40% of children with asthma
had at least 1 residential exposure to a potential asthma trigger. Avoidance
of triggers may be difficult, especially for families who are less socially
mobile and are more likely to live in shared housing environments, such as
apartment buildings. Most intervention trials testing methods to decrease
allergen exposure have focused on dust mite control measures. While individual
studies3 have shown benefit of such strategies,
a recent meta-analysis20 did not confirm evidence
of benefit for all children with asthma based on a subset of studies meeting
strict inclusion criteria.
As part of the baseline evaluation of children with mild to moderate
asthma enrolled in a multicenter trial, the Pediatric Asthma Care Patient
Outcomes Research Team II (PAC PORT II), we questioned families about current
environmental triggers in the home and on actions they routinely take to help
avoid exposures that might exacerbate asthma. Our goals were to assess the
prevalence of exposure to potential environmental triggers, to identify risk
factors for such exposures, and to determine whether instructions to parents
about trigger avoidance were associated with fewer such exposures.
PATIENTS AND METHODS
STUDY POPULATION
We analyzed baseline data from the 638 patients enrolled in the PAC
PORT II, a multicenter randomized trial of asthma care improvement strategies
in practices affiliated with managed care organizations (MCOs) in 3 geographic
areas: Group Health Cooperative, greater Seattle; Rush Prudential Health Plan,
Chicago; and Harvard Pilgrim Health Care and Blue Cross Blue Shield of Massachusetts,
greater Boston. Potential subjects were children aged 3 to 15 years who had
an asthma-related claim for a hospitalization, emergency department visit,
or ambulatory encounter during a 1-year period. Children with a single ambulatory
encounter for asthma also needed to have received 2 or more asthma medications
during the same period to be eligible for screening. Telephone screening then
identified those children who used daily medications for at least 2 months
during a 1-year period as eligible for the trial, and excluded those with
severe asthma or another major chronic illness. The goal of this enrollment
process was to identify children with mild persistent or moderate persistent
asthma, without serious comorbid conditions, for enrollment into the trial.
ANALYSIS
Data were collected using closed-ended questions in face-to-face interviews.
Caregivers reported on their child's asthma symptoms (number of symptom days
based on a 2-week recall), functional status (using the American Academy of
Pediatrics' Children's Health Survey for Asthma),21
and exposure to various environmental triggers in the home. These included
environmental tobacco smoke, dust, pets, and household pests (including cockroaches
and rodents). Key processes of asthma care were examined, including whether
a health care provider "ever gave you written instructions about what to do
about triggers/things that start asthma" and if these were given or updated
in the prior 12 months. A second item asked if a provider, in the past 6 months,
"discussed with you changing things around your childsuch as smoke,
dust, or petsto keep your child from getting asthma symptoms."
For each environmental exposure of interest, we examined differences
by parent-reported patient race or ethnicity, annual family income (<$30 000,
$30 000-$60 000, and >$60 000), and the maximum educational
attainment of either parent in the household (high school education or less,
some posthigh school education, or college graduation). Analyses of
housing type compared those in unattached single family homes with those in
multifamily dwellings. We also assessed differences in relation to reported
symptom frequency. Many subjects were receiving asthma controller medications
at the time of the interview. Because there is no widely accepted standard
for integrating symptom frequency with current medication use in assigning
severity, we categorized patients by symptom days of the past 14 as follows:
0, 1 to 4, 5 to 12, and 13 to 14. These categories approximate the symptom
frequencies of the categories suggested by the National Asthma Education and
Prevention Program guidelines17 but do not
alone classify these patients' "severity."
Categorical variables were analyzed using the 2 test.
To assess associations of reported exposures with demographic factors, we
used separate multivariate logistic regression models for each environmental
trigger. Age, MCO, and the 3 available demographic variables (race, family
income, and parental educational level) were included in all models. Housing
type was tested in all models and retained in final models only if significant
(P<.05). Odds ratios and 95% confidence intervals
(CIs) are reported. Finally, reports of having received written environmental
control instructions or having a discussion with a clinician about such issues
were added to each final model to assess their association with the exposure
of interest. All analyses were performed using SAS statistical software (SAS
Institute Inc, Cary, NC). The study was undertaken with the approval of the
institutional review boards at each of the study sites.
RESULTS
A total of 638 (64%) of the 1000 eligible children identified completed
the baseline interview for the PAC PORT II trial and are described in Table 1. The mean age of enrollees was
9.4 years; 60% were male; and 32% were nonwhite. The families of these patients
were, on average, highly educated, with 89% reporting some college education
for at least 1 member. Patients in the sample varied in their report of current
symptoms, with 33% reporting 5 or more symptom days during the past 14 days.
Patients of the 3 health systems differed according to patient race (P<.001), family income (P =
.005), and parental educational level (P = .01),
but there were no differences in reported symptom frequency across the sites
(P = .39). Symptoms were reported to be more frequent
among lower-income children (P = .04) and varied
by family educational level (P = .04), but did not
differ significantly by patient race (P = .36). Enrollment
rates differed modestly in Boston, Chicago, and Seattle (65%, 69%, and 59%,
respectively; P = .01). Those patients meeting the
eligibility criteria who did not enroll in the study were older (10.3 vs 9.3
years; P<.001), but had a similar illness severity
as measured by the proportion with hospitalizations (P
= .78) or emergency department visits (P = .56) and
the number of weeks taking asthma medications in the past year (P = .57).
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Table 1. Characteristics of the 638 Subjects Enrolled in the PAC PORT
II Trial*
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Exposures to environmental triggers are summarized in Table 2. In 30% of households, at least 1 family member smoked cigarettes
(including 17% of mothers), and 71% of parents expressed worry about their
child's exposure to tobacco smoke. The presence of household pests (including
cockroaches and rodents) was a problem for 18% of the families, including
6% who reported exposure to cockroaches. Furry pets were present in 59% of
households, including 32% with cats and 39% with dogs. Other exposures to
potential environmental triggers included bedroom carpeting in 78% and forced-air
heat in 58% of the households. Most children did not have a plastic cover
on their mattress or pillow. Suboptimal housing attributes such as mildew
or water damage were relatively common. Most patients did not follow recommendations
to wash linen in hot water, and 18% slept with a natural feather pillow.
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Table 2. Parent-Reported Exposure to Potential Environmental Triggers
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Bivariate analyses of selected environmental exposures are shown in Table 3. Smoking in the home was inversely
associated with income (47% vs 19% in the lowest and highest income groups,
respectively, P<.001). Smoking rates also differed
(P<.001) among those not graduating from high
school (51%), those with some college (41%), and college graduates (18%),
but not with patient race or current symptoms. Smoking was more common among
residents of multifamily dwellings (43% vs 27%, P<.001).
Cat and dog ownership were least frequent among families of black patients,
and dogs were most prevalent among families with annual incomes between $30 000
and $60 000 (P<.01). Dog ownership was more
frequent in single family homes. Exposure to household pests was more commonly
reported by black families and those in multifamily dwellings, with trends
toward less exposure among those with a lower family income (P = .07) and lower parental educational attainment (P = .05). Conversely, bedroom carpeting was more frequent in the homes
of white children compared with black and Hispanic or Spanish children. There
were no associations between symptoms and these environmental exposures.
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Table 3. Relationship of Selected Environmental Exposures to Patient
Race, Symptoms, Annual Family Income, and Parental Educational Level
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Consistent with membership in an MCO, virtually all patients reported
having a primary care provider (Table 4). Some aspects of asthma care recommended by the National Asthma
Education and Prevention Program were followed in most patients with asthma.
For example, 70% had their peak expiratory flow measured in the physician's
office at least once and 73% reported owning a spacer device for inhaled medications.
Finally, 91% reported being shown how to use a metered-dose inhaler by a health
professional. Most patients reported having received some written instructions
for taking medications; however, the proportion of patients ever receiving
a written action plan for the management of their asthma was only 21%. Forty-five
percent reported ever receiving written instructions regarding trigger avoidance,
but only 11% reported receiving such instructions in the past year. Forty-two
percent reported a discussion with a health care professional about changing
potential triggers in the home environment in the past 6 months.
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Table 4. Selected Processes of Asthma Care Among the 638 Enrolled Children
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In multivariate models (Table 5),
independent predictors of smoking in the household included an annual family
income of less than $30 000 (OR, 1.9; 95% CI, 1.0-3.7) and between $30 000
and $60 000 (OR, 1.8; 95% CI, 1.1-2.8) compared with greater than $60 000,
and parental educational attainment of high school or less (OR, 4.5; 95% CI,
2.4-8.2) or some college (OR, 2.8; 95% CI, 1.8-4.3) compared with college
graduates. Dog ownership was more likely with parental educational attainment
of high school or less (OR, 2.3; 95% CI, 1.2-4.3) or some college (OR, 1.6;
95% CI, 1.1-2.5) compared with college graduates. Black patients were less
likely than others to own cats (OR, 0.26; 95% CI, 0.12-0.6) or dogs (OR, 0.4;
95% CI, 0.2-0.7). Reports of pests were significantly increased for black
children compared with white children (OR, 2.3; 95% CI, 1.2-4.2). Finally,
black race was associated with lower rates of exposure to carpeting (OR, 0.5;
95% CI, 0.3-0.9).
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Table 5. Independent Demographic Predictors of Environmental Exposures
Among Children With Asthma Using Multivariate Logistic Regression*
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Receipt of written instructions regarding environmental exposures did
not differ significantly by family income (P = .25)
or parental educational attainment (P = .06), but
was more frequently reported by black patients compared with white patients
(56% vs 44%; P = .02). This difference did not persist
after controlling for MCO and age. After controlling for demographic variables,
parental report of having been given written environmental instructions in
the past year was not associated with differential exposure to environmental
triggers. A report of having discussed these issues was positively associated
with having a smoker in the home, but not with the other environmental exposures
when examined in multivariate models.
COMMENT
Recent asthma care improvement efforts have focused predominantly on
appropriate pharmacotherapy, but guidelines17
also recommend patient education to minimize potential environmental triggers.
We sought to determine the prevalence of exposures to potential environmental
triggers for children in their homes, whether parents reported being given
clear instructions about how to avoid them, and whether such instructions
were associated with fewer exposures. We found concerning rates of exposure
to many of the agents known to be potent triggers for some children with asthma.
Of the children in our sample with asthma, 30% were exposed to tobacco smoke
at home, many homes had dogs or cats, and 18% reported household pests, such
as cockroaches. As important as the substantial rates of these exposures was
the finding that only 11% had received written instructions about environmental
trigger avoidance in the past year, although more (42%) reported some discussion
with a physician on these issues in the prior 6 months.
These rates of specific exposures are higher than those recently reported
by the National Health and Nutrition Examination Survey.19
For example, smoking and pet ownership were more common in our study than
in the nationally representative sample. Demographic factors were associated
with differential risk for some of these triggers. Lower family income and
parental educational level were associated with exposure to environmental
tobacco smoke, and black race was associated with lower rates of exposure
to furry pets and bedroom carpeting. We believe strongly that physicians should
not use these data to make assumptions about the home environment of patients
they see. Rather, they highlight the prevalence of exposures to potential
environmental triggers in all socioeconomic strata and among all racial and
ethnic groups. Structured approaches to asking each family with asthma about
their home environment are necessary to tailor educational efforts.
Some triggers more closely linked to housing may be difficult for families
to change. The rate of exposure to cockroaches, 6% by parental report in our
sample, was much lower than that in a study11
of inner-city patients with asthma that measured antigens in the home. Previous
work22 has highlighted the discrepancy between
parental report of specific environmental exposures and antigen levels measured
in the home. Cockroach antigen has been reported to be 33 times more prevalent
in high-poverty areas.23 Likewise, the rate
of reported exposure to rodents was lower in our sample than in the National
Cooperative Inner-City Asthma Study.24 In that
study, which collected household samples from enrolled subjects, detectable
mouse antigen was found in at least 1 room in 95% of the homes.
In the dissemination of the National Asthma Education and Prevention
Program recommendations, the primary focus has been on improving pharmacologic
treatment of asthma by increasing the appropriate use of anti-inflammatory
agents for all patients with persistent asthma.17
This reflects the change in our understanding of asthma as a disease of chronic
inflammation.25-26 Less attention
has been paid to helping families reduce exposure to environmental triggers.
As physicians and patients treat asthma more aggressively, it will be increasingly
important to reduce offending environmental agents to minimize the medications
required.
The lack of association we found between specific exposures and current
symptoms bears comment. First, we did not control for medication use by these
patients, which may reduce some of the symptoms attributable to these exposures.
However, it is also clear that we still have an incomplete understanding of
the contribution to symptoms of environmental exposures among the general
population of children with asthma. Lanphear et al19
suggest that the elimination of residential risk factors could lower asthma
prevalence by 39%, if the associations they report are causally related to
the development of disease. However, we believe it is not possible, given
the cross-sectional studies that make up most of the literature, to accurately
assess such contributions.
The finding that so few patients reported receiving current written
suggestions regarding environmental control is disappointing, but not surprising.
These data reflect parental report of education by clinicians before initiation
of any structured intervention by the PAC PORT II study. We have no information
about the content of such education, which likely varied by clinician within
these practices. Providing parental education is time-consuming for health
care providers. Unless care delivery systems are designed specifically to
provide high-quality patient education, such goals are hard to achieve in
the context of usual primary care visits. A combination of educational materials
(print, videotape, and computer based) may be used, but all require additional
time and effort to ensure comprehension and tailor education to a particular
child and family.
The patients interviewed were enrolled in MCOs with relatively diverse
memberships in 3 geographic areas. These data represent an insured sample
whose socioeconomic status was relatively high, and may not be generalizable
to other regions of the country or to publicly insured or uninsured populations.
Subjects from the 3 sites differed demographically, as did crude rates of
exposure to several of the environmental triggers. We cannot determine whether
this reflects geographic differences, urban vs suburban residence, or attributes
of members of particular plans. Unadjusted reports of prior parental education
also differed among the 3 sites. This study was not designed to compare care
processes among the participating health plans; therefore, we have controlled
for MCO site in multivariate analyses, but do not report effect estimates
for each site.
These data were collected as baseline information for a 2-year randomized
trial of care improvement strategies, which may further limit their generalizability.
Families choosing to participate might differ from those who would not have
enrolled in such a trial. The inclusion criteria aimed to select children
with mild to moderate persistent disease, so these results may not be representative
for children with less severe asthma. Finally, we have no confirmation of
parental reports of either exposure or process-of-care variables. There may
be reluctance for parents (especially those with a child who has asthma) to
accurately report their smoking habits or the presence of household pests.
However, our high rates of these reported exposures argue against such intentional
underreporting. Also, parental recall about education they received may be
incomplete.
Environmental exposures that may add substantially to the morbidity
of children with asthma continue to be prevalent across diverse geographic
and sociodemographic populations. The extent to which these exposures are
responsible for the high morbidity of asthma in low-income areas and minority
populations is unclear. The associations reported herein between particular
environmental exposures and patient race or ethnicity do not imply that such
demographic attributes cause increased exposure. Rather, race, family income,
and parental educational level are crude proxies for a complex set of societal
forces that may affect the prevalence and severity of asthma, the quality
of care received for this condition, and the risk of exposure to potential
asthma triggers. For example, Litonjua et al27
recently showed that a large fraction of the racial and ethnic differences
in asthma prevalence could be explained by area of residence, income, and
level of education. In our data, varying combinations of race, income, and
education were independently associated with exposures. We report ORs for
each of these variables for completeness and consistency. It is a weakness
of this study that we did not obtain more detailed measures of poverty, including
housing attributes, or more detailed data on ethnicity. It is possible that
such additional variables might have better explained the variation in exposure
rates than the demographic variables reported herein.
Some of these environmental exposures, especially those associated with
urban substandard housing, may be difficult for families to mitigate. Others,
such as exposure to tobacco smoke in the home, are recognized threats by most
parents. Although smoking cessation is a challenge in any circumstance, interventions
have attempted to leverage a child's asthma as a motivating factor.28 Programs for structured asthma education that include
trigger avoidance and enhanced self-management have been developed, but have
shown mixed results.29-32
In an era of ever-tightening health care finances, MCOs and practicing physicians
may have difficulty implementing such programs without clear evidence of their
effectiveness in various health care delivery systems. As we continue to develop
new and better pharmacologic agents for asthma, we should also focus on testing
behaviorally oriented strategies through which nonpharmacologic recommendations
of national guidelines might be more widely implemented.
| What This Study Adds
Asthma research, policy statements, and guidelines all highlight the
contribution of indoor environmental exposures to morbidity from childhood
asthma. Environmental tobacco smoke has been shown to be particularly noxious
to children with asthma.
This cross-sectional study reports on the range of exposures reported
by families of children with asthma. Although the specific exposures varied
by sociodemographic factors, children from all backgrounds and circumstances
had exposures of significant concern. These results confirm the need to further
develop effective patient education strategies to reduce indoor environmental
exposures.
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AUTHOR INFORMATION
Accepted for publication November 14, 2001.
This study was supported by grant HS08368 from the US Agency for Healthcare
Quality and Research, Rockville, Md (PAC PORT II); and grant HS08368 from
the National Heart, Lung, and Blood Institute, Bethesda, Md.
We thank Scott Weiss, MD, and Vincent Carey, PhD, for their helpful
comments on manuscript drafts; Nancy Laranjo for data analysis; and the families
who participated in this study in Chicago, Boston, and Seattle.
Corresponding author: Jonathan A. Finkelstein, MD, MPH, Department
of Ambulatory Care and Prevention, Harvard Medical School and Harvard Pilgrim
Health Care, 133 Brookline Ave, Sixth Floor, Boston, MA 02215 (e-mail: Jonathan_Finkelstein{at}harvardpilgrim.org).
From the Department of Ambulatory Care and Prevention, Harvard Medical
School and Harvard Pilgrim Health Care, and the Department of Pediatrics,
Harvard Medical School, Boston, Mass (Dr Finkelstein); the Channing Laboratory,
Brigham and Women's Hospital, Boston (Dr Fuhlbrigge); the Center for Health
Studies, Group Health Cooperative, Seattle, Wash (Dr Lozano); Departments
of Immunology/Microbiology and Pediatrics, Rush-Presbyterian-St Luke's Medical
Center (Dr Grant), the Rush Prudential Health Plan (Dr Shulruff), and the
Center for Healthcare Studies and Division of General Medicine, Department
of Medicine, Northwestern University Medical School (Dr Weiss), Chicago, Ill;
and the Midwest Center for Health Services and Policy Research, Hines VA Hospital,
Hines, Ill (Ms Arduino and Dr Weiss).
REFERENCES
 |  |
1. Mannino DM, Homa DM, Pertowski CA, et al. Surveillance for asthma: United States, 1960-1995. Mor Mortal Wkly Rep CDC Surveill Summ. 1998;47:1-27.
2. Weitzman M, Gortmaker SL, Sobol AM, Perrin JM. Recent trends in the prevalence and severity of childhood asthma. JAMA. 1992;268:2673-2677.
FREE FULL TEXT
3. Platts-Mills TA, Vervloet D, Thomas WR, Aalberse RC, Chapman MD. Indoor allergens and asthma: report of the Third International Workshop. J Allergy Clin Immunol. 1997;100(pt 1):S2-S24.
4. Platts-Mills TAE, Carter MC. Asthma and indoor exposure to allergens. N Engl J Med. 1997;336:1382-1384.
FREE FULL TEXT
5. Committee on the Assessment of Asthma and Indoor Air, US Institute
of Medicine. Clearing the Air: Asthma and Indoor Air Exposures. Washington, DC: National Academy Press; 2000.
6. Weitzman M, Gortmaker S, Walker DK, Sobol A. Maternal smoking and childhood asthma. Pediatrics. 1990;85:505-511.
FREE FULL TEXT
7. Martinez FD, Cline M, Burrows B. Increased incidence of asthma in children of smoking mothers. Pediatrics. 1992;89:21-26.
FREE FULL TEXT
8. Stoddard JJ, Miller T. Impact of parental smoking on the prevalence of wheezing respiratory
illness in children. Am J Epidemiol. 1995;141:96-102.
FREE FULL TEXT
9. Cook DG, Strachan DP. Summary of effects of parental smoking on the respiratory health of
children and implication for research. Thorax. 1999;54:357-366.
FREE FULL TEXT
10. Sporik R, Holgate ST, Platts-Mills TAE, Cogswell JJ. Exposure to house-dust mite allergen (Der p I) and the development
of asthma in childhood. N Engl J Med. 1990;323:502-507.
ABSTRACT
11. Rosenstreich DL, Eggleston PA, Kattan M, et al. The role of cockroach allergy and exposure to cockroach allergen in
causing morbidity among inner-city children with asthma. N Engl J Med. 1997;336:1356-1363.
FREE FULL TEXT
12. Kang BC, Johnson J, Veres-Thorner C. Atopic profile of inner-city asthma with a comparative analysis on
the cockroach-sensitive and ragweed-sensitive subgroups. J Allergy Clin Immunol. 1993;92:802-811.
FULL TEXT
|
ISI
| PUBMED
13. Ingram JM, Sporik R, Rose G, Honsinger R, Chapman MD, Platts-Mills TA. Quantitative assessment of exposure to dog (Can f 1) and cat (Fel d
1) allergens: relation to sensitization and asthma among children living in
Los Alamos, New Mexico. J Allergy Clin Immunol. 1995;96:449-456.
FULL TEXT
|
ISI
| PUBMED
14. Phipatanakul W, Eggleston PA, Wright EC, Wood RA. Mouse allergen, II: the relationship of mouse allergen exposure to
mouse sensitization and asthma morbidity in inner-city children with asthma. J Allergy Clin Immunol. 2000;106:1075-1080.
FULL TEXT
|
ISI
| PUBMED
15. Nelson HS, Szefler SJ, Jacobs J, Huss K, Shapiro G, Sternberg AL. The relationships among environmental allergen sensitization, allergen
exposure, pulmonary function, and bronchial hyperresponsiveness in the Childhood
Asthma Management Program. J Allergy Clin Immunol. 1999;104:775-785.
FULL TEXT
|
ISI
| PUBMED
16. National Asthma Education Program. Guidelines for the Diagnosis and Management of Asthma. Bethesda, Md: National Institutes of Health; 1991. Publication 91-3042.
17. National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the Diagnosis
and Management of Asthma. Bethesda, Md: National Institutes of Health; 1997. Publication 97-4051.
18. Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention:
NHLBI/WHO Workshop Report March 1993. Bethesda, Md: National Institutes of Health; 1995. Publication 95-3659.
19. Lanphear BP, Aligne CA, Auinger P, Weitzman M, Byrd RS. Residential exposures associated with asthma in US children. Pediatrics. 2001;107:505-511.
FREE FULL TEXT
20. Gotzshe PC, Johansen HK, Burr ML, Hammarquist C. House dust mite control measures for asthma [Cochrane Review on CD-ROM]. Oxford, England: Cochrane Library, Update Software; 2001:issue 4.
21. Asmussen L, Olson LM, Grason HA, Fagan J, Weiss KB. Reliability and validity of the Children's Health Survey for Asthma. Pediatrics. 2001;104:e71. Available at: http://www.pediatrics.org.
Accessed December 19, 2001.
22. Chew GL, Burge HA, Dockery DW, Muilenberg ML, Weiss ST, Gold DR. Limitations of a home characteristics questionnaire as a predictor
of indoor allergen levels. Am J Respir Crit Care Med. 1998;157:1536-1541.
FREE FULL TEXT
23. Kitch BT, Chew G, Burge HA, et al. Socioeconomic predictors of high allergen levels in homes in the greater
Boston area. Environ Health Perspect. 2000;108:301-307.
ISI
| PUBMED
24. Phipatanakul W, Eggleston PA, Wright EC, Wood RA. Mouse allergen, I: the prevalence of mouse allergen in inner-city homes:
the National Cooperative Inner-City Asthma Study. J Allergy Clin Immunol. 2000;106:1070-1074.
FULL TEXT
|
ISI
| PUBMED
25. Barnes PJ. A new approach to the treatment of asthma. N Engl J Med. 1989;321:1517-1527.
ABSTRACT
26. Lemanske RF, Busse WW. Asthma. JAMA. 1997;278:1855-1873.
FREE FULL TEXT
27. Litonjua AA, Carey VJ, Weiss ST, Gold DR. Race, socioeconomic factors, and area of residence are associated with
asthma prevalence. Pediatr Pulmonol. 1999;28:394-401.
FULL TEXT
|
ISI
| PUBMED
28. Irvine L, Crombie IK, Clark RA, et al. Advising parents of asthmatic children on passive smoking: randomised
controlled trial. BMJ. 1999;318:1456-1459.
FREE FULL TEXT
29. Lewis CE, Rachelefsky G, Lewis MA, de la Sota A, Kaplan M. A randomized trial of ACT (Asthma Care Training) for kids. Pediatrics. 1984;74:478-486.
FREE FULL TEXT
30. Greineder DK, Loane KC, Parks P. A randomized controlled trial of a pediatric asthma outreach program. J Allergy Clin Immunol. 1999;103:436-440.
FULL TEXT
|
ISI
| PUBMED
31. Bernard-Bonnin A, Stachenko S, Bonin D, Charette C, Rousseau E. Self-management teaching programs and morbidity of pediatric asthma:
a meta-analysis. J Allergy Clin Immunol. 1995;95:34-41.
FULL TEXT
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32. Wilson SR, Latini D, Starr NJ, et al. Education of parents of infants and very young children with asthma:
a developmental evaluation of the Wee Wheezers program. J Asthma. 1996;33:239-254.
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