Abstract and Introduction
by C. Warren Bierman, MD, University of Washington
November 7, 2003
Abstract
Dust mites, cockroaches, cats, dogs and other animals, mold,
and cigarette smoke all contribute to the etiology of atopic asthma.
Decreasing exposure to these factors can reduce the symptoms of active
disease. House dust mites are found in 99% of homes, and cat and dog
antigens are found in 100% of homes -- even in those without resident
pets. In addition, mold spores and, in houses of lower socioeconomic
groups, cockroach antigens, are frequently found. Acaricides, chemicals
that kill mites, are troublesome because of their potential toxicity.
Tannic acid, a protein denaturing agent commonly found in tea, has been
shown to reduce allergen levels in house dust. Individuals who have
never had a cat may become allergic by exposure to cat allergen from
other sources. Cat owners with allergies to their pets are frequently
unwilling to recognize a causal relationship and give up the cat.
Although dogs can be a potent source of allergens, most studies have
reported that children have fewer symptoms as a result of exposure to
dog allergens than cat allergens. Passive smoke exposure from parents
who smoke is associated with respiratory symptoms in infants and
toddlers. Controlled studies have proven that measures to control
environmental factors in asthma -- such as vinyl zippered covers on
bedsheets, HEPA filters on air vents, and removal of carpets from floors
or pets from the home -- can be effective in reducing the number of
asthmatic episodes and in reducing the overall incidence of asthma.
Introduction In a study of allergy clinic patients in Baltimore,
Maryland[1,2] and a case control study of patients presenting
to an emergency room with acute asthma in Wilmington, Delaware,[3]
house dust mites were found by immunochemical methods in 99% of homes
occupied by allergic patients. Cat and dog antigens were found in 100%
of homes -- even in homes that did not have these resident pets. In
addition, mold spores and, in houses of lower socioeconomic groups,
cockroach antigens were found.
Dust mites, cockroaches, cats, dogs and other animals, mold, and
cigarette smoke all contribute to the etiology of atopic asthma.
Decreasing exposure to these factors can reduce the symptoms of active
disease and decrease the likelihood of asthma. In addition to
medication, control of the environment is a significant step in treating
atopic asthma.
The Allergens Many allergens present in house dust have been identified
and include acarids, such as Dermatophagoides species; insects,
such as cockroaches; domestic animals, such as cats; fungi and air
pollutants, such as cigarette smoke (Table I).
House dust mites. Worldwide, investigators have found that the
dust mite (Fig. 1) is a significant cause of allergic respiratory
disease. Dekker[4] first related the mite to asthma in 1928,
after he found substantial quantities present in house dust. However, it
was not until 1964[5,6] that Dermatophagoides species
were confirmed as a source of allergens present in house dust-- dust
collected by vacuuming the bedding of allergic patients was found to
contain dust mites on light microscopy. Patients improved when they were
removed from contact with the mites, and reacted on bronchial challenges
with bronchoconstriction.

Photomicrograph of a house dust mite. Reprinted with permission from
Paul J. Beggs, Macquarie University.
In September, 1987,[7] an international workshop on dust
mites reviewed the epidemiology, immunochemistry, and molecular biology
of the arachnid, as well as the human immune response to it and
strategies to avoid exposure and the subsequent immune reaction. A
second workshop, which addressed the taxonomy of mites, as well as
standardized the techniques for sampling floor, furniture, or bedding
dust, was held in 1990.[8] They summarized that the three
methods for determining exposure are mite counts, assay of mite
allergens and measurement of guanine. A quantitative assay for guanine
has been reported to demonstrate a good correlation with assay of Group
I mite antigen. A semi-quantitative assay for guanine (ACAREX test) may
be a useful screening test for clinical practice. For allergen assays in
research work, the guanine test should continue to be used.
The Dermatophagoides species of mites are sightless, eight-legged
animals about 0.33 mm in length. As members of the Acaridae family, they
are close relatives of the spider. The mite does not take in fluid
through a mouthpiece or probiscus, but instead is equipped with a
special organ that extracts water from the air. They may be found in
soft toys,[9] curtains, clothing, bedding, mattresses,
carpets, and upholstered furniture.[10] The two most relevant
species in the US are D pteronyssinus and D farinae,[11]
and two others -- Blomia tropicalis and Euroglyphus maynei
-- are present in the Gulf Coast, where they are give rise two medically
significant allergens.[12]
Dust mites grow optimally at a temperature of 21.1°C (70° F). Cold
winters reduce their population and, hence, decrease mite sensitization
in individuals with asthma and allergy. Charpin and associates[13]
found that the prevalence of asthma with positive skin tests to house
dust mites was significantly lower in mountain school children living in
the Alps than in those residing on the Mediterranean coast. To kill
mites by washing, the water temperature must be greater than 54.4°C
(130° F). The dry cleaning process is also effective in eliminating
mites.[14]
Specifically, the fecal pellets of the mite contain the allergenic
proteins. The allergens persist months after eradication of live mites.[11]
Because the fecal pellets are large, they remain aerosolized for only a
few minutes after they are stirred from a resting place. The possibility
for exposure, therefore, is best studied by measuring mite allergen in
dust vacuumed from surfaces.
Dust samples from bedding, carpets and sofas were studied on a seasonal
scale in Charlottesville, Virginia, by Platts-Mills and coworkers.[15]
The levels of mite allergen were found to rise in July, with the highest
level occurring from August to December with a peak in October.
Acaricides, chemicals which kill mites, are troublesome because of their
potential toxicity. Of the acaricides, only benzyl benzoate, which is
used to treat scabies, is sold in the US. It is available as a moist
powder preparation under the brand name Acarosan. Tannic acid, a
protein denaturing agent commonly found in tea, has been shown to reduce
allergen levels in house dust,[10] but it does not eliminate
mites. This agent is also available in the US.
Cockroaches. Cockroach allergen is a major problem for inner city
children with asthma.[16] Findings from a number of recent
studies suggested that cockroach allergens are a major indoor air
allergen in the Eastern US and Hawaii, particularly among the poor.[3]
Both cockroach fecal extracts and whole body extracts are associated
with positive skin tests, and it has been concluded that fecal matter
may be the most medically significant allergen,[17] because
this material is likely to crumble and become disseminated as airborne
dust. In a study conducted by Pollart and colleagues,[18] the
highest levels of Bla g 2, a major cockroach antigen, were found in
kitchen floor dust, but the antigen could also be detected in other
sites in the home. Bronchial challenge studies[19] performed
on 10 asthmatic adults who were positive to cockroach on skin testing,
induced an attack of asthma in each.
In an urban dormitory infected with German cockroaches, Sarpong and
colleagues[20] collected dust from 18 bedrooms and 5
kitchens, 2 weeks before extermination and 2 weeks after. Before
extermination, the median level of Bla g 2 antigen was 5.2 U/g; 2 weeks
after extermination, medium levels fell to 0.95 U/g. Presumably other
cockroach components were present, but only Bla g II was identified by
study design. Longitudinal studies to determine how often extermination
should be carried out to maintain low allergen levels should be
conducted. Such studies might be undertaken in the homes of patients
with positive cockroach antigen skin tests.
Cockroaches of three species are common in the US: German, American, and
Oriental. Specific allergens have been purified only for the first two.
The highest concentration of their allergens are found in food areas.
Professional extermination is needed to eliminate them when these are
found in multifamily dwellings, because repopulation occurs from other
roach colonies elsewhere in the building. Tannic acid works to denature
cockroach antigens, but does not kill the roaches themselves.
Cats. The fact that cat allergens can cause asthma has been
confirmed by studies in a special cat challenge room.[21] A
monoclonal antibody for measuring a major cat allergen, Fel d I, has
been used since 1988 in a series of studies of cat allergy.[22]
Cat allergens are found in homes with cats, and are capable of inducing
symptoms in sensitive patients.[23] Cat allergen has also
been found in dust samples from homes without cats, and from every other
building source where it has been looked for, though the levels in
buildings without cats are much lower than those in homes with cats.[24]
After removing a cat from a house in which it has lived, it may take 15
to 40 weeks before airborne allergen is no longer present.[25]
Individuals who have never had a cat may become allergic by exposure to
the allergen from contact with cats belonging to others.
Cat allergens occur in small particles less than 4mcm in diameter and
can remain airborne for many hours.
Cat owners with allergies to their pets are frequently unwilling to
recognize a causal relationship and give up their cat.[26] If
one is unwilling to remove the cat, the following strategies may reduce
the amount of allergen to which the devoted owner is exposed:[27]
Dogs. Although dogs can be a
potent source of allergens, most studies report that children have fewer
symptoms as a result of dog allergens than cat allergens. In a study of
children with asthma, 1 in 10 reacted to cat allergens, whereas only 1
in 100 reacted to dog allergens.[28] In general, more
individuals own dogs than cats. However, intimacy of exposure may be a
factor -- cats more often than dogs go into the house and into the
bedroom of children. Research on dogs has been hampered by the lack of
identified allergens. Recently, a monoclonal antibody against a dog
antigen has been isolated. Studies using that antibody will provide more
information about dog antigens and their importance in the house.
Other animals. Rabbits, mice, rats, hamsters, guinea pigs and
birds have been implicated in the induction of allergic reactions.
Positive skin tests can prompt the removal of the inciting animal from
the house, because patients are more willing to give up these smaller
animals than they are to give up cats and dogs, who may be considered
part of the family.
Molds. Molds can always be cultured from samples of house dust,
particularly from samples collected in moist areas. The presence of mold
may even be detected by smell in some rooms. Growth of molds on hard
surfaces can be controlled by chemicals, such as a bleach solution, but
these are not suitable for carpeting or old books, paper, and firewood.
Many people react to molds by skin test, but the importance of this is
not certain. Some allergens are not present in spores (ie, Asp fl) and
some spores cannot be separated one from the other (ie, Penicillium
sp and Aspergillus sp). Regularly cultured spores include
Penicillium, Aspergillus, (Fig. 2) and Cladosporium.
Avoidance measures are hard to evaluate -- these molds are present
year-round in temperate zones in the outside air. Avoidance measures
depend on strategies to inhibit mold growth indoors.

Photomicrograph of the Ascomycete, Aspergillus fumigatus showing conidiophores, (A) and conidia, the asexual reproductive spores, (B). Reprinted with permission from Steve Kagen, MD (www.allernet.com).
Tobacco smoke.
Passive smoke exposure from parents who smoke is associated with
respiratory symptoms in infants and toddlers who present to the
emergency department with wheezing.[29] The risk of
developing asthma is 2.5 times greater in young children with mothers
who smoke 10 or more cigarettes/day indoors compared with mothers who
don't smoke or who smoke less than 10 cigarettes/day. The recent
increases in the prevalence and severity of childhood asthma may be
attributable in part to the increase in the prevalence of smoking among
mothers.
In a study of children of all ages, those living in a smoking household
were found to be 63% more likely to have asthma than those residing in a
nonsmoking household.[29] Among 415 nonsmoking asthmatic
children seen consecutively, asthma symptoms were more severe if the
mother smoked. Boys were more sensitive to passive smoking than were
girls, and the adverse effects increased with age and duration of
exposure.[30] In a survey of more than 7,000 children and
adolescents under 18 years of age, those whose mothers smoked were more
likely to experience wheezing respiratory illness than children with
nonsmoking mothers. The investigators estimate that maternal smoking is
responsible for 380,000 cases of childhood asthma.[31]
Avoidance Measures The complete eradication of mites and other allergens
is not possible, but homes should be constructed with an air space
between the ground and the floor, or with a basement. In more humid
parts of the country this space between the ground and the floor should
be covered with 5-mil (5-mil is the thickness designation used by
hardware stores, who may also sell 1-mil plastic sheeting.) black
plastic sheeting or concrete. Basements should be covered with vinyl
tile or there should be an air space between the cement floor and the
carpeting. Moisture leaks should be corrected, leaking roofs repaired,
and insulation placed in walls that tend to be cold. A dehumidifier may
help those basements which tend to be humid. Various mildew-resistant
paints are available, but should not be used on radiators because the
mildew side may be toxic when airborne. Whenever black mildew appears,
it should be controlled by chlorine-containing solutions that may be
sprayed on tiles or impermeable surfaces.
Heating and cooling systems. If one has forced air heat,
electrostatic filters attached to the furnace can remove effectively the
majority of mite particles and other airborne allergens. These
disposable filters should be changed at least monthly and the ducts
should be cleaned yearly. Baseboard or wall heaters should be vacuumed
weekly to remove particles of dust mites and other allergens, as well as
the lint in which they may be trapped. Relative humidity should be kept
below 45%, sufficiently low so that there is no condensation on cold
window frames, but not so low that one generates a static electric spark
on walking across a synthetic carpet. Mites and molds grow better with
humidity over 45%.[32]
Cleaning carpets and upholstery. A central vacuum system which
exhausts outside or vacuum cleaning regularly with a double thickness
filter bag is helpful in removing accumulated dust from carpets, but it
does not remove embedded allergens or mites. Since vacuuming increases
the aerosolization of dust particles for a short time, the allergic
individual should not engage in this activity, or should wear a dust
mask when doing so. The allergic patient should have exhaust fans in his
bathroom and over the stove that lead outside and use them regularly
when bathing or when boiling water on the stove.
Steam cleaning of carpeting and upholstery may reduce mite allergen
levels for as long as a month, but will not reduce mite numbers deep in
the material. Cold shampooing actually may increase mite numbers by
providing moisture. The most effective method to eradicate mites is to
remove carpeting and to replace it with hardwood and vinyl flooring, as
previously noted.
Allergen control in the bedroom. Though plastic mattress covers
are readily available, they are uncomfortable. A more comfortable
barrier between the patient and the mattress mites are encasings that
breathe and do not crinkle, which may be purchased from any one of a
number of allergy supply houses. Sheets and pillow cases should be
changed weekly and washed in water of 54.4°C (130° F), and blankets
should be laundered every 2 to 4 weeks. If a room air filter is to be
used, it should be a HEPA air filter. Electrostatic room filters release
ozone which can cause pulmonary inflammation. Likewise, vaporizers
increase the number of mites by providing moisture, and should not be
used. Clothing should be placed in a closet with the door closed. Cats
and dogs should never be permitted in the bedroom and should be removed
from the household if possible. Also, cigarette smoking in the house and
car should be prohibited.
Effects of Environmental Control In 1983, Murray and Ferguson[33]
published the results of a study that they conducted on children who had
asthma and were skin prick positive to mite antigen. An experimental
group of 10 children were provided with zippered vinyl covers for
pillows, mattresses, and box springs. Carpets were removed from the
bedroom. If the children showed positive reactions to pets, they were
removed from the house. A control group of 10 other children were
treated with pharmacotherapy and given general dust control measures but
did not have specific instructions concerning bedding or carpets. In one
month, the investigators found that those children in the experimental
setting had a four-fold increase in tolerance to histamine on
bronchoprovocation, whereas the 10 children in the control group had
decreased tolerance. Days on which wheezing occurred were substantially
less for those children in the experimental group than in the control
group. Medication requirements also differed -- only five doses of
albuterol were required by the experimental group, while 224 doses of
albuterol, theophylline and/or prednisone were used by the control
group.
Similarly, the effect of treating the mattress and bedroom with benzyl
benzoate, placebo or 3% tannic acid were compared.[34]
Mattresses and pillows were covered with impermeable covers in the
tannic acid group, and the benzyl benzoate group was used as the control
group. Reduction in mite allergen by 98% occurred in the tannic acid
group compared with the benzyl benzoate and control groups. In another
study, 67 children were followed by Sporik and colleagues for 11 years.[35]
Of the 17 subjects who had a diagnosis of asthma, most were allergic to
house dust mites. The investigators concluded that active asthma in any
child was 4.8 times greater if he or she was exposed to more than 10mg
of Der p I, the Dermatophagoide antigen, per gram of dust.
Editorial Comment - Environmental Control of Asthma Dr. Bierman has
provided an elegant description of household environmental allergens,
their potential significance, and control measures. He has included in
this review the potentially harmful respiratory effects of tobacco smoke
as an environmental pollutant. While control measures for all of these
are easy to describe, they are often challenging to implement. The
environmental polluting effects of tobacco smoke may be the easiest to
eliminate because this not only doesn't cost the family but actually
provides an increase in disposable income by removing the expense of
cigarette purchase. There should therefore never be any hesitancy in
strongly recommending the cessation of smoking or at least the
elimination of indoor (or in-car) cigarette smoking. Measures to control
household allergen exposure, however, can be expensive and disruptive.
Moreover, in contrast to the effects of cigarette smoking, which causes
a general risk to the user and passive recipients of tobacco smoke,
allergen exposure presents a risk only to the sensitized individual.
Individuals with asthma or rhinitis have differing sensitivities and
differing degrees of disease severity. These issues must be considered
in the decision-making process for prescription of environmental control
recommendations. Just as with the prescribing of medications, there are
cost -effectiveness concerns that need to be addressed.
Recommendations to remove a beloved pet from the home, to tear up
carpeting, or even the more modest recommendation to cover mattresses
and pillows, require an appropriate assessment in order to have a
reasonable level of confidence that there will be therapeutic benefit.
This assessment requires identification of the presence of IgE antibody
specific to household environmental allergens, a clinical evaluation of
the degree to which the specific allergen contributes to the symptoms,
and an assessment of the severity of the disease.
Allergy skin testing or appropriate in vitro tests such as the
radioallergosorbent test (RAST) for inhalant allergens is therefore
essential for intelligent prescribing of environmental allergen control.
However, the consequent identification of IgE antibody specific to a
household allergen provides no information regarding whether that
allergen actually contributes to the disease and certainly provides no
information regarding the degree to which it contributes or the disease
severity. These are clinical judgments made by assessment of the history
following identification of the immunologic sensitivity.
Let us examine some clinical examples of decision-making related to
environmental control prescribing:
Example 1: An 8-year-old boy has severe chronic asthma that has
resulted in multiple hospitalizations despite vigorous pharmacologic
measures. While his symptoms occur year-round, they are noted to
increase markedly in the fall when the forced-air furnace first begins
to operate and when a vacuum cleaner is being operated in his presence.
Allergy skin testing shows a large wheal and flare to dust mite with a
negative diluent control.
In this case, it is clear that maximal effort should be expended for
dust mite control measures. The clinical significance of the specific
IgE demonstrated by skin testing is convincingly supported by the
history.
Example 2: An 8-year-old boy has chronic asthma that is
well-controlled with 200 mcg twice-daily of inhaled beclomethasone
diproprionate. Although daily wheezing and coughing had been previously
present, he now has infrequent albuterol inhaler requirements; there is
no interference with sleep; exercise tolerance is normal so long as he
uses his albuterol inhaler prior to vigorous activity; and pulmonary
function testing is completely normal. He describes only vigorous
exercise, exposure to cats, and getting a cold as identifiable triggers
for his symptoms. He has a dog but no cat, nor has a cat ever been in
his house. He describes no increase in symptoms even with close contact
with the dog. The dog is an 8-year-old Collie who is dearly beloved by
the patient and his siblings. Allergy skin testing showed positive skin
tests to multiple outdoor inhalant allergens, dust mite, indoor molds,
and cat. Skin test to dog was negative by puncture but weakly positive
to a 1000 PNU/mL intradermal.
This case is obviously more complicated than the first. While there is
considerable IgE antibody to inhalant allergens, the history gives few
clues that provide a high level of confidence that environmental control
measures will provide substantial benefit, especially since the patient
is now well-controlled on an acceptably safe and convenient medical
regimen. While implementation of simple low-cost measures to his bedroom
environment to decrease dust mite exposure may be reasonable, it is
difficult to justify high-cost measures or the removal of the beloved
family pet. While an argument can be made that continued exposure may
eventually increase sensitivity to the dog and dust mite resulting in
worsening symptoms, it is difficult to estimate the likelihood of that
possibility. This is clearly not a decision where the physician can
justifiably be dogmatic (no pun intended) in recommendations. The family
should be made aware of available data, potential concerns, and
potential reservations concerning the effectiveness of expensive and
disruptive environmental control measures so that they can make an
informed decision.
Example 3: An 8-year-old boy has episodic asthma with viral
respiratory infections. This has resulted in periods of coughing and
wheezing with only temporary relief from an albuterol inhaler until a
short course of prednisone is administered. While the patient had
required hospitalization on several occasions for this when he was
younger, the last hospitalization was 3 years ago. He has noticed no
cough, wheeze, or nasal symptoms between the 3 acute episodes associated
with colds during the past year. His exercise tolerance is normal
between the symptomatic episodes. He has a dog and cat, lives in an old
musty-smelling house with a damp basement on his parents' farm. His skin
tests showed a degree of reactivity to dust mite, dog, cat, molds, and
pollens.
Here we have a case where clearly considerable cost and little benefit
would be expected from environmental control measures for inhalant
allergen. Despite the presence of specific IgE to dust mite, there is no
suggestion of chronic or environmentally-triggered symptoms. His
medication requirements consist only of vigorous intervention measures
during the viral-URI induced exacerbations. While the possibility of
increased symptoms from continuous exposure to dust mite cannot be
excluded, there appears little justification for expending the expense
and effort for environmental control measures at present.
These three examples illustrate some of the complexities of
decision-making regarding the implementation of environmental controls
described by Dr. Bierman. Vigorous measures -- even if disruptive and
expensive -- are well-justified in the first case, equivocal in the
second, and are almost certainly not warranted in the third case,
despite at least the potential for clinical problems from the specific
IgE to environmental allergens identified. Just as medication needs to
be tailored to the needs of the individual, so should the prescription
for environmental control measures be tempered by consideration of the
clinical need, potential for benefit, and cost, both economic and
social.
Miles M. Weinberger, MD
Department of Pediatric Allergy
University of Iowa Hospital
Iowa City, Iowa
Tables Table I - Allergens Identified in House Dust in the United States
| Acarids |
| Dermatophagoides |
| D
pteronyssinus (Der p I, Der p II)* |
| D
farinae (Der f I, Der f II) |
| Euroglyphus
maynei (Euro m I) |
| Blomia
tropicalis |
| Insects |
|
Cockroaches (Bla g I, Bla g II) |
| Blatella
germanica |
| Domestic
animals |
| Cat (Fel d
I) |
| Dog (Can f
I) |
| Fungi |
| Penicillium |
| Aspergillus |
| Cladosporium |
| Air
pollutants |
| Cigarette
smoke |
| Others |
| Pollen |
| Wild mice
and rats |
| Other pets |
| * |
Specific antigens are
listed in (brackets). |
Adapted from WB Saunders Company.
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