Environmental Health Perspectives Volume
103, Supplement 6, September 1995
[Citation
in PubMed]
Indoor Air Pollution and Childhood Asthma: Effective Environmental Interventions
Ruth A. Etzel
Air Pollution and Respiratory Health Branch, National Center for Environmental
Health, Centers for Disease Control and Prevention, Atlanta, Georgia
Abstract
Exposure to indoor air pollutants such as tobacco smoke and dust mites
may exacerbate childhood asthma. Environmental interventions to reduce exposures
to these pollutants can help prevent exacerbations of the disease. Among
the most important interventions is the elimination of environmental tobacco
smoke from the environments of children with asthma. However, the effectiveness
of reducing asthmatic children's exposure to environmental tobacco smoke
on the severity of their symptoms has not yet been systematically evaluated.
Dust mite reduction is another helpful environmental intervention. This
can be achieved by enclosing the child's mattresses, blankets, and pillows
in zippered polyurethane-coated casings. Primary prevention of asthma is
not as well understood. It is anticipated that efforts to reduce smoking
during pregnancy could reduce the incidence of asthma in children. European
studies have suggested that reducing exposure to food and house dust mite
antigens during lactation and for the first 12 months of life diminished
the development of allergic disorders in infants with high total IgE in
the cord blood and a family history of atopy. Many children with asthma
and their families are not receiving adequate counseling about environmental
interventions from health care providers or other sources. -- Environ
Health Perspect 103(Suppl 6):55-58 (1995)
Key words: asthma, air pollution, passive smoking, childhood,
interventions
This article was presented at the Symposium on Preventing
Child Exposures to Environmental Hazards: Research and Policy Issues held
18-19 March 1994 in Washington, DC.
Address correspondence to Dr. Ruth A. Etzel, Chief, Air
Pollution and Respiratory Health Branch, National Center for Environmental
Health, Centers for Disease Control and Prevention, 4770 Buford Highway,
NE, Mail Stop F-39, Atlanta, GA 30341-3724. Telephone (404) 488-7320. Fax
(404) 488-7335.
Introduction
The environment in which a child lives may contribute to a child's risk
of having ongoing exacerbations of asthma. There is also some evidence that
the environment contributes to a child's risk of developing asthma. Much
of the early evidence that there was a significant environmental component
to asthma came from studies of twins. Edfors-Lubs studied 6996 twin pairs
in the Swedish twin registry and found that when one monozygotic twin had
asthma, the other twin had it 19% of the time (1). She concluded
that the remaining 81% were due to environmental factors. Among dizygotic
twins, if one twin had asthma, the other twin had it only 4.8% of the time.
Thus, she reasoned, although there are certainly genetic factors involved,
there is clearly an important environmental component to developing asthma.
Asthma prevalence is higher among African American children than among
white children (2,3). Furthermore, African American children have
higher rates of hospitalization for asthma, but much of this increase is
thought to be due to poverty rather than to race (4,5). It is not
known whether children who live in poverty are more heavily exposed to indoor
air pollutants than children who do not live in poverty.
In the United States, children spend most of their time (average, 20
hr) indoors (6). Therefore, in addition to considering the effects
of outdoor air pollution (7), it is important to take into account
the effects that exposure to indoor air pollutants may have on childhood
asthma. The dominant allergens associated with asthma are found indoors,
i.e., mite, cat, dog, and cockroach (8,9). Some have hypothesized
that the increased prevalence of asthma among children may be a manifestation
of an increase in children's sensitization to inhaled allergens (10,11).
Higher concentrations of tobacco smoke and pesticides are also found indoors
(12,13). This article will review primary and secondary prevention
of asthma, focusing on interventions for reducing tobacco smoke and indoor
allergens, and will provide some information about the possible role of
pesticides.
Prevention of Asthma
To date, most of the asthma interventions have been designed to prevent
asthma exacerbations (known as secondary prevention); few efforts to prevent
the development of asthma (known as primary prevention) have been undertaken.
Because it is the more common approach, secondary prevention will be discussed
first, followed by primary prevention.
Secondary Prevention: Passive Smoking
Secondary prevention includes efforts to prevent asthma exacerbations,
such as household interventions to eliminate cigarette smoke from the child's
environment. Children with asthma who have a parent who smokes have more
frequent exacerbations and more severe symptoms (14-27). Table 1
summarizes recent epidemiologic studies of the effects of passive smoking
on asthma in childhood. Despite the importance of exposure to environmental
tobacco smoke for asthmatic children, the effectiveness of reducing children's
exposure to environmental tobacco smoke has not been systematically evaluated.
In the only intervention among asthmatic children reported in the literature,
Murray and Morrison reported that if parents expose their asthmatic children
to less cigarette smoke, their asthmatic symptoms will be less severe (21).
However, this study's conclusions are limited by the investigators' inability
to measure exposure to environmental tobacco smoke and the subjective assessment
of severity of symptoms. Additional studies of the effectiveness of reducing
asthmatic children's exposure to environmental tobacco smoke are needed.
Secondary Prevention: Dust Mite Elimination
Secondary prevention also includes household interventions to eliminate
dust mites. Among the most effective measures to decrease mite infestation
are plastic mattress covers. Ehnert and her colleagues performed a randomized
controlled trial of two dust-mite elimination procedures in the bedrooms
of 24 children with asthma (28). In group one, mattresses, blankets,
and pillows were enclosed in polyurethane-coated casings and bedroom carpets
were treated with tannic acid at the start of the study and at months 4
and 8. In group two, mattresses and carpets were treated with the acaricide,
benzyl benzoate (BB) at the start of the study and at months 4 and 8. A
third group received treatment of mattresses and carpets with placebo foam
at the start of the study and at months 4 and 8. There was a significant
decrease in concentrations of mite allergen on mattresses covered by polyurethane
casings, while there was no significant reduction of mite allergen
on mattresses treated with BB or placebo foam. In addition, the children
whose mattresses were enclosed in polyurethane casings showed a significant
reduction of bronchial hyperreactivity after 8 months. Unfortunately, this
study did not test the effectiveness of polyurethane casings alone, but
in combination with other measures.
Murray and Ferguson did a controlled trial among 20 asthmatic children
with positive skin-prick tests to either house dust or Dermatophagoides
farinae (29). The experimental group was given zippered vinyl
covers for pillows, mattresses, and box springs and instructed to launder
the curtains and wash blankets and mattress pads every two weeks. The control
group was not instructed to make any changes in the child's bedroom. After
one month, children in the experimental group had fewer days on which wheezing
was observed, medication was administered, or an abnormally low PEFR was
recorded. In the experimental group, the bronchial responsiveness to inhaled
histamine decreased 4-fold, while it increased 2-fold in those in the control
group.
Comprehensive reviews of environmental controls in the management of
lung disease have been published by Samet (30) and Ingram and Heymann
(31).
Primary Prevention
Primary prevention of asthma is the prevention of the development of
asthma in young children. In utero exposure to tobacco-smoke products
has been shown to be an important determinant of wheezing in the first
year of life (20). Thus primary prevention of asthma should include
efforts to reduce smoking during pregnancy. No studies to date have investigated
whether asthma incidence can be reduced by decreasing smoking during pregnancy.
Swedish investigators have studied the usefulness of screening cord blood
for IgE at birth. They report that 75% of infants with a high cord blood
IgE will develop atopic diseases by 1 year of age and 82% of newborn infants
with high cord blood IgE will develop atopic symptoms before 7 years of
age (32,33). Under the assumptions that preventive measures can delay
the onset of atopic allergies by an average of 8 months and reduce existing
treatment costs within the 6-year period by about 10% (and assuming total
patient compliance) then IgE screening of all newborn infants or infants
with a family history of atopic disease in Sweden is cost effective (34).
They found that using family history of atopic disease alone as a screening
test is not cost effective. The investigators estimated that an IgE screening
program in Sweden would result in a total cost savings for atopic allergies
before 6 years of age of approximately 20 million Swedish crowns or 3 million
U.S. dollars per year. Because these assumptions and results may be different
in the United States, similar studies should be undertaken in this country.
Hide and his colleagues did a randomized controlled trial of infants
with a family history of atopy and high cord total IgE. In the experimental
group, lactating mothers avoided milk, eggs, fish, and nuts; and infants
avoided soya, wheat, and orange for the first 12 months of life (35).
All infants in the experimental group slept on polyvinyl-covered mattresses,
and acaricide foam and powder were applied to the infants' bedroom carpet,
living room carpet, and upholstered furniture every three months. At age
12 months, 4 of 58 infants in the experimental group had signs of asthma
compared to 12 of 62 infants in the control group. At age 2 years, 4 of
43 infants in the experimental group had asthma, compared with 9 of 41 infants
in the control group (36). The authors concluded that reducing the
exposure to food and house-dust mite antigens diminished the development
of allergic disorders in high-risk infants in the first 2 years of
life. It would be useful to test each of these interventions separately
to find out which has a more important effect.
Future Research Needs: Pesticides and Asthma
There is currently no evidence of a link between indoor exposure to pesticides
and exacerbations of childhood asthma. Evidence of a link between pesticides
and asthma is largely limited to anecdotal reports of asthma among adults.
Bryant (36) described two patients in whom asthma was reportedly
precipitated by exposure to synthetic organophosphates. Occupational asthma
has been reported in a worker producing the fungicide, captafol (37);
in a woman cleaner working with a carpet fungicide, tributyl tin oxide (38);
in a farmer using the fungicide tetrachloroisophthalonitrile in his plastic
greenhouse (39); and among farm workers spraying crops with organophosphate
pesticides containing carbamates and phosphorodithioates (40).
A cross-sectional study was conducted in Saskatchewan, Canada, to investigate
the association of self-reported asthma and pesticide use in 1939 crop farmers
(41). Each farmer participating in the study completed a questionnaire
about history of employment; respiratory health; working conditions; cigarette
smoking; and use of pesticides, herbicides, and fertilizers. The prevalence
of asthma was associated with the use of carbamate insecticides (OR = 1.8,
95% CI: 1.1 to 3.1, p = 0.02).
Shim and Williams (42) reported that 51 of 60 adult patients with
asthma claimed that exposure to pesticides worsened their asthma. The most
frequently mentioned source of the insecticide exposure was fumigation of
the house or apartment or roach sprays. One limitation of this study is
that the histories of patients' exposures were not verified.
Newton and Breslin studied seven patients with histories of worsening
asthma due to exposure to a widely used aerosol insecticide spray. Under
controlled conditions, they were exposed to concentrations up to 6.7 mg/l,
and lung functions were measured after the exposure. Chest tightness was
reported by all of them after being exposed to the insecticide, but objective
evidence of airway obstruction was present in only one, who showed a greater
than 20% fall in FEV1, compared to his baseline value; two showed a very
small decline in the maximum midexpiratory flow rate (43).
Does indoor exposure to pesticides cause exacerbation of asthma among
children? Although there is little objective evidence, this exposure may
deserve further investigation.
Summary
Exposure to indoor air pollutants such as tobacco smoke and dust mites
may exacerbate asthma, and effective measures to prevent exposures to these
pollutants are available. However, it appears that many children and their
families, particularly those who rely on emergency rooms as their primary
source of care, are not receiving adequate counseling from health care providers
or other sources. Improvement of the health status of children with asthma
requires a public health approach that emphasizes disease prevention rather
than the traditional medical approach. Success in improving the health status
of children with asthma will not be possible without addressing the predominant
social, cultural, and environmental conditions in which children live.
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