Avoiding Asthma Triggers

Abstract and Introduction
by C. Warren Bierman, MD, University of Washington
November 7, 2003
Alterneria
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.

References

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    Dr. Bierman, Department of Pediatrics, University of Washington, Seattle, Wash

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