Exposure Settings

The indoor exposures considered in this report are highly dependent on the characteristics of the outdoor and indoor environment and its occupants. For example, house dust mites are a very common exposure in temperate and humid regions. They are found primarily within residences, concentrated in the bedroom. Cockroaches, which also thrive in temperate and humid regions, are an important exposure in some urban environments. They are found primarily near food sources. Fungi are ubiquitous and have been the primary source of allergen for several studied populations. Endotoxins may be found in humidifiers and in bacteria from other indoor, as well as outdoor sources. In some environments, exposure to animal allergens; molds; environmental tobacco smoke (ETS); indoor combustion products; and chemicals used in cleaning, building materials, and furnishings may be important. Many of these pollutants are also present in outdoor air, and indoor exposures can result from the infiltration of outdoor air into buildings.

Indoor Air Exposures and Asthma Exacerbation

Studies of asthma can be divided into those dealing with factors leading to the development of asthma and those dealing with factors that exacerbate the illness in known asthmatics. Most of the research on this topic addresses “asthma exacerbation,” the onset or worsening of symptoms—some combination of shortness of breath, cough, wheezing, and chest tightness—in someone who already has developed asthma.

Epidemiologic investigations, challenge studies, and clinical experience have yielded solid information on the potential for many indoor exposures to exacerbate asthma. The committee found sufficient evidence to conclude that there is a causal relationship between

• exposure to the allergens produced by cats, cockroaches, and house dust mites, and exacerbations of asthma in sensitized individuals; and
• ETS exposure and exacerbations of asthma in preschoolaged children.

There is sufficient evidence of an association between several exposures and exacerbations of asthma. Dog allergen exposure is associated with exacerbation of asthma in individuals specifically sensitized to these allergens. Fungal exposure is associated with exacerbation in sensitized asthmatics and may be associated with nonspecific chest symptoms. Research indicates that rhinovirus infection is associated with wheezing and exacerbations in asthmatics. There is also sufficient evidence to conclude that brief high-level¹ exposures to NO₂ and increased airway responses among asthmatic subjects to both nonspecific chemical irritants and inhaled allergens.

Damp conditions are associated with the presence of symptoms considered to reflect asthma; symptom prevalence among asthmatics is also related to dampness indicators. The factors related to dampness that may actually lead to asthma exacerbation are not yet confirmed, but probably relate to dust mite and fungal allergens. There is sufficient evidence that some nonresidential buildings provide exposures that exacerbate asthma. However, the specific agents responsible for such exacerbations are as yet unstudied.

Limited or suggestive evidence was found for an association between exposures to domestic birds and exacerbation of asthma, although it is unclear what portion of this association is attributable to an allergic asthmatic response to the mites harbored by these birds. There is also limited or suggestive evidence of a relationship between

• exposure to the infectious agents respiratory syncytial virus (RSV), Chlamydia pneumoniae, and Mycoplasma pneumoniae, and exacerbation of asthma;
• chronic ETS exposure and exacerbation of asthma in older children and adults;
• acute ETS exposure and exacerbation of asthma in individuals responsive to this exposure;
• nonacute, nonoccupational formaldehyde exposure and wheezing and other respiratory symptoms; and
• exposure to certain fragrances and the manifestation of respiratory symptoms in asthmatics sensitive to such exposures.

Inadequate or insufficient information was identified to determine whether or not exacerbations of asthma result from nonacute, nonoccupational exposures to cow, horse, and rodent allergens; endotoxins; houseplants² or cut flowers; the bacterial agent Chlamydia trachomatis; pesticides; plasticizers; and volatile organic compounds (VOCs) other than formaldehyde. Some of these same agents do or may play a role in asthma resulting from exposures in occupational settings, a topic outside the purview of this study.

Although there is sufficient evidence to conclude that pollen exposure is associated with exacerbation of existing asthma in sensitized individuals, and pollen allergens have been documented in both dust and indoor air, there is inadequate or insufficient information to determine whether indoor exposure to pollen is associated with exacerbations of asthma.

These findings are summarized in Table 2.

TABLE 2

Summary of Findings Regarding the Association Between Indoor Biologic and Chemical Exposures and the Exacerbation of Asthma in Sensitive Individuals.

Indoor Air Exposures and Asthma Development

The second outcome reviewed by the committee was the development of asthma—the initial onset of the illness. Asthma is defined by the manifestation of a set of symptoms rather than by any one objective test. With asthma symptoms ranging from clearly episodic to nearly continuous, from mild to severe, and from coughing without other respiratory symptoms to a loud wheeze, the initial diagnosis of the illness can be complicated and subject to controversy. It is thus difficult to study the determinants of and influences on asthma development. An additional complication stems from the fact that some of the most provocative evidence regarding development comes from studies of infants. Prior to the age of approximately 3, children may exhibit symptoms that are characteristic of asthma, but they may not exhibit persistent asthmatic symptoms or other related conditions such as bronchial reactivity or allergy later in life. Chapter 1 discusses the definitions of asthma and the characteristics of its clinical presentation.

Saying that a particular agent may be associated with the development of asthma does not mean it is the sole factor determining whether an individual will manifest the illness. Most scientists believe that some individuals have a prior, underlying predisposition that permits the evolution of clinical asthma. The development of this predisposition to asthma is dependent on a complex—and at present poorly understood—combination of factors, which are partially inherited and partially acquired later in life.

After careful consideration of the scientific literature, the committee concluded there is sufficient evidence of a causal relationship between exposure to house dust mite allergen and the development of asthma in susceptible children. This conclusion was based on the preponderance of several lines of evidence, including the results of clinical studies and population-based, case-control, and prospective epidemiologic investigations; the consistency of the association in different racial and ethnic groups; and the presence of a dose–response relationship between exposure to dust mite allergen and sensitization. Chapter 5 delineates the reasoning underlying this conclusion in greater detail.

There is sufficient evidence to conclude that there is an association between ETS exposure and the development of asthma in younger children. In the limited number of studies that have been able to separate the effects of maternal active smoking during pregnancy from the effects of ETS exposure after birth, evidence suggests that—although both exposures are detrimental— maternal smoking during pregnancy has the stronger adverse effect.

Limited or suggestive evidence exists for associations between

• cockroach allergen exposure and development of asthma in preschool-aged children; and
• infection with RSV and development of asthma in pre-school-aged children.

The impact of exposure to these agents has been the subject of great research interest in the past few years, and efforts presently under way may clarify their role in asthma development.

Published case reports, public health surveillance of physician reporting, and cross-sectional studies of building occupants with indoor air quality complaints also provide limited or suggestive evidence of an association between aspects of the nonindustrial indoor environment and the development of asthma, with a building occupancy-related pattern of symptoms and in some instances objective abnormalities. What is lacking for the most part, however, is knowledge of specific etiologic agents in these nonindustrial indoor environments that might be responsible for new work-related asthma cases.

Inadequate or insufficient evidence exists to determine whether or not the other indoor exposures listed in Table 1 are associated with the development of asthma. This lack of information points to a gap in present-day knowledge concerning asthma—one that will be challenging to resolve.

There is limited or suggestive evidence of no association between infection with rhinovirus—the medical term for the large and ubiquitous group of viruses responsible for a variety of respiratory infections including those referred to as “the common cold”—and asthma development.

Table 3 summarizes these findings.

TABLE 3

Summary of Findings Regarding the Association Between Indoor Biologic and Chemical Exposures and the Development of Asthma.

Effectiveness of Indoor Environmental Interventions in Limiting Exposures and Affecting Asthma Outcomes

Patients with asthma and the parents of children with asthma need reliable information on which measures are likely to be most effective for improving indoor air quality. Specific recommendations are found in each chapter but there are general principles that should be kept in mind. Agents that can exacerbate asthma may generally be thought of in two categories: specific allergens and nonspecific respiratory tract irritants. Exposure to nonspecific irritants, such as cigarette smoke, may lead to asthma symptoms in any person with asthma; while allergens are only problems for individuals who are allergic to them. For example, if a person with asthma is allergic to cats, exposure to cats may cause wheezing; but if that person is not allergic to cats, exposure to them will not cause any problems. Therefore, reducing indoor airborne exposure to irritants is likely to help all asthmatic individuals to some degree while reductions in allergen exposure would only be expected to help individuals who are allergic to the allergens being reduced.

While the report identifies a number a mitigation strategies that are or may be effective in reducing exposure to potentially problematic agents, the committee found only a small number for which there is presently evidence that proper implementation of the strategy results in an improvement of symptoms or lung function in asthmatics. It is important to remember, though, that the absence of evidence does not mean an absence of effect. The science regarding indoor environmental interventions, exposure limitation, and effects on asthma outcomes is not nearly as well developed as that regarding the health effects of exposures. Exposure assessment³ is often the weakest link in environmental health studies because it is difficult to do and is given inadequate attention by many researchers.

Nonetheless, the committee was able to identify well-conducted, rigorous studies on which to base conclusions.

Sufficient evidence of an association was found between the use of a combination of physical measures and a reduction in indoor dust mite allergen levels in dust samples. As detailed in Chapter 5, strategies for the effective control of mite growth vary by climate. Such measures have been shown to be effective at reducing symptoms in controlled trials and should be part of normal management of asthma in mite-allergic individuals. Several studies now under way are evaluating whether aggressive allergen avoidance regimes have an effect on the subsequent development of asthma. The results of these and other studies will inform the question of whether primary prevention of dust mite-induced asthma is possible. Two related issues that will have to be addressed are (1) the feasibility of implementing such comprehensive interventions and (2) whether these interventions result in lower rates of sensitization to a particular exposure or all exposures.

The committee found limited or suggestive evidence that the combined use of cockroach extermination and control of potential reservoirs of allergen in beds, carpets, furnishings, and clothing through cleaning can achieve a short-term decrease in cockroach allergen levels in indoor environments. Extermination alone appears ineffective because significant allergen levels remain in settled dust; cleaning alone in the absence of complete extermination does not eliminate the sources of the allergen. There was inadequate or insufficient evidence to determine whether or not an association exists between any cockroach mitigation or prevention strategy and transient or long-term improvement of symptoms or lung function in cockroach-allergic asthmatics. However, since evidence does suggest that dust mite mitigation strategies result in improvement of symptoms or lung function, mitigation of cockroach exposures would appear to be a sensible course of action in the absence of more definitive information.

Although the strategy may be unpopular, there is limited or suggestive evidence of an association between removal of a cat from the home and improvement of symptoms or lung function in cat-allergic asthmatics. Concomitant removal or isolation of known reservoirs of cat allergen (carpets, upholstery, mattresses, pillows) may be required to diminish allergen levels to those commonly measured in homes without cats. Limited or suggestive evidence indicates that some measures short of removal (e.g., washing the animal) may result in transient reduction in allergen levels. However, there is inadequate or insufficient evidence to determine whether or not an association exists between measures short of removal of a cat from the home and improvement in symptoms in cat-allergic asthmatics. Data on the effectiveness of interventions for other animals are too sparse to draw informed conclusions.

It is possible to physically remove accessible growing fungi from indoor environments. The entry of fungal spores from outdoors can be substantially reduced in mechanically ventilated buildings by pressurizing them and filtering incoming air; closing windows should also reduce indoor concentrations from outdoor sources. Although there is limited or suggestive evidence that such steps may result in a reduction in the levels of fungi in the indoor environment, the health impact of such reduction has not been studied. Fungi are difficult to kill, and dead fungal material probably contains allergens that can become airborne, although this has not been thoroughly tested.

There is relatively little information on the impact of ventilation and air-cleaning measures on indoor pollen levels, although it is clear that shutting windows and other measures that generally limit the entry rate of unfiltered outdoor air can be effective.

No general conclusions about means of altering exposure to low levels of endotoxin can be made at the present time. However, avoiding the use of cool mist humidifiers would appear to be a simple and effective means of eliminating risk of high-level exposure to endotoxin at home as well as exposure to organisms associated with hypersensitivity pneumonitis.

Source control—that is, stopping smoking—appears to be the only reliably effective means of preventing environmental tobacco smoke exposure. There is sufficient evidence to conclude that increased ventilation is technologically capable of reducing the indoor concentration of ETS particles and gases, and that particle air-cleaning methods are technologically capable of reducing the indoor concentration of ETS particles. However, evidence is lacking on whether interventions designed to encourage the use of the requisite ventilation and air cleaning methods would be associated with a reduction in asthma development or exacerbation.

Control options for chemical and particulate pollutants in indoor environments include source modification (removal, substitution, or emission reduction), ventilation (exhaust or dilution), or pollutant removal (filtration). The various forms of pollutant source modification are usually the most effective. For most gaseous pollutants—NO₂ for example—removal via air cleaning is not presently practical.

No intervention studies clearly document that any form of dampness control works effectively to reduce symptoms or to reduce the chances of asthma development. However, given its relationship to factors (such as dust mites and fungal growth) associated with asthma, steps to reduce dampness may be appropriate. For homes, these measures include powered mechanical ventilation to remove or dilute occupant-generated moisture, proper installation of vapor barriers, channeling ground water away from foundations, sealing below-ground walls to prevent water intrusion, protecting ground-level concrete slabs from moisture intrusion, and constructing crawl spaces to prevent water intrusion.

There are both theoretical evidence and limited empirical data indicating that feasible modifications in ventilation rates can decrease or increase⁴ concentrations of some of the indoor pollutants associated with asthma by up to approximately 75%. Limited or suggestive evidence exists to indicate that particle air cleaning is associated with a reduction in the exacerbation of asthma symptoms. Theoretical and limited empirical data indicate that particle air cleaners are most likely to be effective in reducing the exacerbation of asthma symptoms associated with particles smaller than approximately 2 µm, such as ETS particles⁵ and some airborne cat allergen. There is insufficient evidence to determine whether or not the use of particle air cleaners is associated with decreased asthma development. It should also be noted that microorganisms can grow on some air-cleaning equipment such as filter media; thus, improperly maintained air cleaners are also a potential source of indoor pollutants.

Inadequate or insufficient information was available regarding several other interventions. These are discussed in Chapters 5 through 10.

It is difficult to draw general conclusions regarding effective indoor environmental interventions. However, the committee is able to offer some observations. For many allergens, effective strategies consist of integrated approaches consistently applied over time. The two primary components of an integrated approach are (1) removal or cleaning of allergen reservoirs and (2) control of new sources of exposure. Source removal—where it is possible—is typically the most effective control measure and may be the only effective measure for some agents. Avoidance of exposure through source removal, substitution, or emission reduction is usually the most successful approach for chemical agents.