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EXECUTIVE SUMMARY I he statistics are disturbing The Centers for Disease Control and Prevention (CDC) esti- mates that asthma affected about 17.3 million individuals in the United States in 1998. It is the most common chronic illness among children in the United States and one of the most common chronic illnesses overall in the country. Although by many mea- sures the health of Americans is improving, CDC notes the self- reported prevalence rate for asthma increased 75°/O from 1980 to 1994. Studies show that asthma mortality is disproportionately high among African Americans and in urban areas that are char- acterized by high levels of poverty and minority populations. Nor is the phenomenon limited to the United States. The prevalence of asthma in some other parts of the world including Australia, New Zealand, Ireland, and the United Kingdom exceeds that of the United States. Researchers have wondered whether the indoor environment may play a role in the increasing asthma problem. There is ample justification for this speculation. We know, for example, that indi- viduals spend nearly all of their time indoors most of it in their own homes and that many of the exposures thought to be asso- ciated with asthma occur predominately indoors. If the indoor 1
2 CLEARING THE AIR environment plays a role, then interventions to limit or eliminate exposures there have the potential to help asthmatics and per- haps result in primary prevention of the illness. Against this backdrop, the U.S. Environmental Protection Agency (EPA) is developing an outreach strategy focused on re- ducing asthma-related morbidity and mortality potentially asso- ciated with exposure to indoor environments. To help ensure that such efforts are based on sound science, EPA requested that the National Academies undertake an assessment of asthma and its relationship to indoor air quality. The EPA charged the committee with two primary objectives: 1. To provide the scientific and technical basis for communi- cations to the public on the health impacts of indoor pollutants related to asthma, and mitigation and prevention strategies to re- duce these pollutants. 2. To help determine what research is needed in these areas. This report presents the results of that assessment. ORGANIZATION AND FRAMEWORK The content of this report reflects the committee's goal to speak to a wide-ranging audience of science, health, and engi- neering professionals; government officials; and interested mem- bers of the public. The material presented thus covers a broad range of topics in order to establish a common base of knowledge for the reader. The scope of this material is far too vast for any one book to deal with comprehensively. Other publications, cited throughout the report, go into greater detail on specific issues. The major topics addressed in the report are the following: · the definition of asthma and the characteristics of its clini cal presentation (Chapter 1~; · methodologic issues in evaluating the evidence regarding indoor air exposures and asthma, including the categorizations used to summarize the evidence and the framework for consider- ing exposure to indoor sources (Chapter 2~;
EXECUTIVE SUMMARY TABLE 1 Indoor Exposures Aclclressecl in This Report 3 Animals Cats Dogs Rodents Cows and horses Domestic birds Cockroaches House dust mites Endotoxins NO2, NOx~nitrogen oxides) Pesticides Ozone* Particulate matter with sources other than ETS* SO2, SOx (sulfur oxides) * Biological Chemical Fungi or molds Houseplants Pollen Infectious agents Rhinovirus Respiratory syncytial virus Chlamydia trachomatis Chlamydia pneumonias Mycoplasma pneumonias Plasticizers Volatile organic compounds Formaldehyde Fragrances Environmental Tobacco Smoke (ETS) *An outdoor air pollutant potentially associated with asthma that can penetrate the indoor environment and that may in some cases have indoor sources. Since the committee's mandate was to address indoor air pollutants, the discussion of this agent is less detailed than others in the report and no conclusions are drawn concerning outdoor exposures and asthma outcomes. . patterns of asthma morbidity and mortality (Chapter 3); · the pathophysiology of asthma that is, the molecular mechanisms that underlie the structural and functional changes in the lungs and airways of asthmatics (Chapter 4~; · the committee's review of the state of the scientific litera- ture regarding indoor air exposures and the exacerbation and de- velopment of asthma Table 1 lists the biologic and chemical ex- posures addressed in this report. (Chapters 5-7~; · the scientific literature on general exposures in indoor en- vironments (Chapters 8-9~; and · how indoor exposures to pollutants associated with the in- cidence or symptoms of asthma are affected by building ventila- tion and particle air cleaning (Chapter 10~.
4 CLEARING THE AIR The committee faced a significant challenge in conducting its review research on asthma is burgeoning and significant new papers are constantly being published. Although the committee did its best to paint an accurate picture of the state of the science at the time the report was completed, it is inevitable that research advances will overtake its conclusions. i] CONCLUSIONS ABOUT THE RELATIONSHIP BETWEEN INDOOR EXPOSURES AND ASTHMA The committee used a uniform set of categories to summarize its conclusions regarding the association between exposure to an indoor agent and asthma development and exacerbation, and the effectiveness of exposure mitigation and prevention measures. Box 1 lists the definitions of these categories. The distinctions among categories reflect the committee's judgment of the overall strength, quality, and persuasiveness of the scientific literature evaluated. Chapter 2 details the methodologic considerations un- derlying the categorizations and their definitions. The sections below are a synopsis of the committee's find- ngs. Chapters 5 through 10 address the reasoning underlying the conclusions and present the findings in greater detail. Exposure Settings The indoor exposures considered in this report are highly de- pendent on the characteristics of the outdoor and indoor environ- ment 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 popula- tions. Endotoxins may be found in humidifiers and in bacteria from other indoor, as well as outdoor sources. In some environ ments, exposure to animal allergens; molds; environmental to- bacco smoke (ETS); indoor combustion products; and chemicals used in cleaning, building materials, and furnishings may be im
EXECUTIVE SUMMARY 5
6 CLEARING THE AIR portent. 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 fac- tors 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 short- ness of breath, cough, wheezing, and chest tightness in some- one 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 rela- tionship 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 preschool- aged children. There is sufficient evidence of an association between sev- eral exposures and exacerbations of asthma. Dog allergen expo- sure is associated with exacerbation of asthma in individuals spe- cifically 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 exacer- bations in asthmatics. There is also sufficient evidence to conclude that brief high-level~ exposures to NO2 and increased airway re- sponses among asthmatic subjects to both nonspecific chemical irritants and inhaled allergens. iAt concentrations that may occur only when gas appliances are used in poorly ventilated kitchens.
EXECUTIVE SUMMARY 7 Damp conditions are associated with the presence of symp- toms considered to reflect asthma; symptom prevalence among asthmatics is also related to dampness indicators. The factors re- lated 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 attribut- able to an allergic asthmatic response to the mites harbored by these birds. There is also limited or suggestive evidence of a rela- tionship between · exposure to the infectious agents respiratory syncytial vi- rus (RSV), Chiamydia pneumonias, and Mycoplasma pneumonias, and exacerbation of asthma; · chronic ETS exposure and exacerbation of asthma in older children and adults; · acute ETS exposure and exacerbation of asthma in indi- viduals responsive to this exposure; · nonacute, nonoccupational formaldehyde exposure and wheezing and other respiratory symptoms; and · exposure to certain fragrances and the manifestation of res- piratory symptoms in asthmatics sensitive to such exposures. Inadequate or insufficient information was identified to de- termine 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 Chiamydia 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 2Mites and fungi associated with houseplants could be involved in asthma out- comes but no studies document this connection.
8 CLEARING THE AIR 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 docu- mented in both dust and indoor air, there is inadequate or insuffi- cient information to determine whether indoor exposure to pollen is associated with exacerbations of asthma. These findings are summarized in Table 2. Indoor Air Exposures and Asthma Development The second outcome reviewed by the committee was the de- velopment 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 determi- nants of and influences on asthma development. An additional complication stems from the fact that some of the most provoca- tive evidence regarding development comes from studies of in- fants. Prior to the age of approximately 3, children may exhibit symptoms that are characteristic of asthma, but they may not ex- hibit persistent asthmatic symptoms or other related conditions such as bronchial reactivity or allergy later in life. Chapter 1 dis- cusses the definitions of asthma and the characteristics of its clini- cal presentation. Saying that a particular agent may be associated with the de- velopment of asthma does not mean it is the sole factor determin- ing whether an individual will manifest the illness. Most scien- tists 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 fac- tors, which are partially inherited and partially acquired later in life. After careful consideration of the scientific literature, the com
EXECUTIVE SUMMARY TABLE 2 Summary of Finclings Regarcling the Association Between Indoor Biologic and Chemical Exposures and the Exacerbation of Asthma in Sensitive Inclivicluals 9 Biological Agents Chemical Agents Sufficient Evidence of a Causal Relationship Cat Cockroach House Dust Mite Sufficient Evidence of an Association Dog Fungi or molds Rhinovirus ETS (in preschool-aged children) NO2, NOxthigh-level exposures*) Limited or Suggestive Evidence of an Association Domestic birds ETS (in school-aged and older children, and Chlamydia pneumonias Mycoplasma pneumonias Respiratory Syncytial Virus (RSV) in adults) Formaldehyde Fragrances Inadequate or Insufficient Evidence to Determine Whether or Not an Association Exists Cow and horse Pesticides Rodents (as pets or feral animals) Plasticizers Chlamydia trachomatis VOCs Endotoxins Houseplants Pollen exposure in indoor environments Insects other then cockroaches Limited or Suggestive Evidence of No Association (no agents met this definition) kitchens *At concentrations that may occur only when gas appliances are used in poorly ventilated mittee concluded there is sufficient evidence of a causal rela- tionship 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, in- cluding the results of clinical studies and population-based, case- control, and prospective epidemiologic investigations; the consis
10 CLEARING THE AIR tency 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 as- sociation 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 dur- ing pregnancy from the effects of ETS exposure after birth, evi- dence suggests that although both exposures are detrimental- maternal smoking during pregnancy has the stronger adverse effect. Limited or suggestive evidence exists for associations be tween · 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 physi- cian reporting, and cross-sectional studies of building occupants with indoor air quality complaints also provide limited or sug- gestive evidence of an association between aspects of the nonin- dustrial 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 respon- sible 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 informa- tion 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 be
EXECUTIVE SUMMARY 11 tween infection with rhinovirus the medical term for the large and ubiquitous group of viruses responsible for a variety of respi- ratory infections including those referred to as "the common cold" and asthma development. Table 3 summarizes these findings. TABLE 3 Summary of Finclings Regarcling the Association Between Indoor Biologic and Chemical Exposures and the Development of Asthma Biologic Agents Chemical Agents Sufficient Evidence of a Causal Relationship House dust mite Sufficient Evidence of an Association (no agents met this definition) Limited or Suggestive Evidence of an Association Cockroach (in preschool-aged children) Respiratory Syncytial Virus (RSV) Inadequate or Insufficient Evidence to Determine Whether or Not an Association Exists Cat Cow and horse Dog Domestic birds Rodents Cockroaches (except for preschool-aged children) Endotoxins Fungi or molds Chlamydia pneumonias Chlamydia trachomatis Mycoplasma pneumonias Houseplants Pollen Limited or Suggestive Evidence of No Association Rhinovirus (adults) (no agents met this definition) ETS (in preschool-aged children) (no agents met this definition) NO2, NOX Pesticides Plasticizers VOCs Formaldehyde Fragrances ETS (in school-aged and older children, and in adults) (no agents met this definition)
12 CLEARING THE AIR 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 recommenda- tions 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 nonspe- cific irritants, such as cigarette smoke, may lead to asthma symp- toms in any person with asthma; while allergens are only prob- lems 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 air- borne exposure to irritants is likely to help all asthmatic individu- als to some degree while reductions in allergen exposure would only be expected to help individuals who are allergic to the aller- gens 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 Jung func- tion in asthmatics. It is important to remember, though, that the absence of evidence does not mean an absence of effect. The sci- ence 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. Expo- sure assessments is often the weakest link in environmental health studies because it is difficult to do and is given inadequate attention by many researchers. Classically, "exposure assessment" involves specifying the population that might be exposed to the agent of concern; identifying the routes through which exposure can occur, and estimating the magnitude, duration, and timing of the dose that individuals might receive as a result of their exposure (NAS, 1994~.
EXECUTIVE SUMMARY 13 Nonetheless, the committee was able to identify well-con- ducted, 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 in- door 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 re- ducing symptoms in controlled trials and should be part of nor- mal management of asthma in mite-allergic individuals. Several studies now under way are evaluating whether aggressive aller- gen avoidance regimes have an effect on the subsequent develop- ment 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 ad- dressed are (1) the feasibility of implementing such comprehen- sive interventions and (2) whether these interventions result in lower rates of sensitization to a particular exposure or all expo sures. The committee found limited or suggestive evidence that the combined use of cockroach extermination and control of poten- tial reservoirs of allergen in beds, carpets, furnishings, and cloth- ing through cleaning can achieve a short-term decrease in cock- roach allergen levels in indoor environments. Extermination alone appears ineffective because significant allergen levels remain in settled dust; cleaning alone in the absence of complete extermina- tion does not eliminate the sources of the allergen. There was in- adequate or insufficient evidence to determine whether or not an association exists between any cockroach mitigation or preven- tion strategy and transient or long-term improvement of symp- toms or Jung function in cockroach-allergic asthmatics. However, since evidence does suggest that dust mite mitigation strategies result in improvement of symptoms or Jung 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 Jung function in cat-allergic asthmatics. Concomitant removal or isolation of known reservoirs of cat allergen (carpets, upholstery, mattresses,
14 CLEARING THE AIR pillows) may be required to diminish allergen levels to those com- monly 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 out- doors can be substantially reduced in mechanically ventilated buildings by pressurizing them and filtering incoming air; clos- ing windows should also reduce indoor concentrations from out- door 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 ma- terial probably contains allergens that can become airborne, al- though this has not been thoroughly tested. There is relatively little information on the impact of ventila- tion and air-cleaning measures on indoor pollen levels, although it is clear that shutting windows and other measures that gener- ally 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. How- ever, avoiding the use of coo! 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 to- bacco 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 in- door concentration of ETS particles. However, evidence is lacking on whether interventions designed to encourage the use of the
EXECUTIVE SUMMARY 15 requisite ventilation and air cleaning methods would be associ- ated with a reduction in asthma development or exacerbation. Control options for chemical and particulate pollutants in indoor environments include source modification (removal, sub- stitution, 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 gas- eous 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 re- duce the chances of asthma development. However, given its re- lationship to factors (such as dust mites and fungal growth) asso- ciated with asthma, steps to reduce dampness may be appropriate. For homes, these measures include powered me- chanical ventilation to remove or dilute occupant-generated mois- ture, proper installation of vapor barriers, channeling ground water away from foundations, sealing below-ground walls to pre- vent water intrusion, protecting ground-level concrete slabs from moisture intrusion, and constructing craw] spaces to prevent wa- ter intrusion. There are both theoretical evidence and limited empirical data indicating that feasible modifications in ventilation rates can de- crease or increased concentrations of some of the indoor pollut- ants associated with asthma by up to approximately 75°/0. Lim- ited 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 indi- cate that particle air cleaners are most likely to be effective in re- ducing the exacerbation of asthma symptoms associated with par- ticles smaller than approximately 2 ,um, 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 associ 4The indoor concentrations of some pollutants from outdoors particulate matter and ozone, for example may increase with the ventilation rate. 5Particle air cleaners are not effective in reducing concentrations of the gaseous components of ETS.
16 CLEARING THE AIR ated 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 regard- ing 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 ap- proach 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 ex- posure through source removal, substitution, or emission reduc- tion is usually the most successful approach for chemical agents. GENERAL RES"RCH RECOMMENDATIONS AND CONCLUSIONS Asthma is a complex illness. The many variables that deter- mine its development and severity defy simple summary. Al- though great strides have been made over the past few years in elucidating mechanisms and understanding the role of environ- mental and genetic influences, much work remains to be done. Importantly, we still do not know whether or to what extent the reported increases in asthma can be attributed to indoor expo sures. Subsequent chapters of this report contain specific recommen- dations for further research on the biologic and chemical agents addressed and on the characteristics of indoor environments that may influence asthma outcomes. A digest of these recommenda- tions is contained in Chapter 11. Some general observations are offered below. The factors that determine the predisposition to sensitivity to certain agents and lead to the development of asthma are still not well understood. There is a great need for studies that rigorously
EXECUTIVE SUMMARY 17 examine the role of prenatal exposure and whether the age of first exposure influences the development of sensitization. The inter- action of different environmental exposures with genetic suscep- tibilities a topic of great interest but little research progress- also has to be pursued. A major problem in choosing and implementing an interven- tion to mitigate an exposure is the generally limited data avail- able. The limitations exist in regard to both the quantity and the quality of research data. Many of the studies reported are not based on rigorous protocols. Definition of clinical outcome (espe- cially in infants), measurement of exposure, rigorous study de- sign, appropriate population selection, and generalizability of the findings are among the issues that are often not adequately ad- dressed. Indoor environments typically include exposures to mul- tiple potentially problematic agents dust mites and fungi, for example, are ubiquitous. It has proven difficult to assess the indi- vidual roles of the factors implicated in existing studies because complete characterization of exposures has not been done. There- fore, it is often not possible to determine with confidence whether any effects noted are indeed the results of specific exposures stud- ied or of confounders. The poor and inner city residents are vulnerable populations for asthma development, morbidity, and mortality. As such, there is great interest in identifying effective means to address preva- lent exposure problems. Although some research on interventions has been directed at these populations, some of the strategies tried may not be practical to implement unless the subjects are part of an organized protocol providing guidance and funds. Further, in- dividuals living in public or rental housing, or in multifamily units, may not have control over parts of their indoor environ- ment that would be desirable to modify, such as carpeting, exces- sive moisture, and comprehensive pest management. Future re- search has to address more effectively the feasibility and generalizability of intervention programs on target populations. Finally, to date there has been little connection between the scientific literature regarding asthma and the scientific literature regarding the characteristics of healthy indoor environments (for example, building design and operation; and sources, transport, control methods, and exposures to indoor pollutants). Relatively
18 CLEARING THE AIR little of the existing medical and epidemiologic literature on asthma quantifies indoor environmental conditions such as hu- midity, ventilation, and pollutant concentrations or exposures in sufficient detail. The effectiveness of exposure limitation strate- gies in reducing exposures and asthma development or exacerba- tion has, in general, been inadequately studied. These are areas of research that have the potential to impact public health signifi- cantly. The committee believes that better communication be- tween medical, public health, behavioral science, engineering, and building professionals is likely to result in more informed studies on the causes of asthma and the means to limit problem- atic exposures. The committee encourages efforts to bring these groups together to educate one another on their areas of exper- tise. Although considerable work has been done and is being done on asthma per se, increased research efforts are needed to address the characteristics of healthy indoor environments. Asthma re- search clearly needs interdisciplinary involvement not only of clinicians, immunologists, and researchers in related biologic ar- eas but also of engineers, architects, materials manufacturers and others who are responsible for the design and function of indoor environments. Collaborations should be fostered, and con- sideration should be given to formulating mode! research proto- cols that include indoor environmental characteristics. REFERENCES Benson V, Marano MA. 1998. Current estimates from the National Health Interview Survey, 1995. National Center for Health Statistics. Vital Health Statistics Series 10 No. 199. DHHS Publication PHS 98-1527. Carr W. Zeitel L, Weiss K.1992. Variations in asthma hospitalizations and deaths in New York City. American Journal of Public Health 82:59-65. Lang DM, Polansky M. 1994. Patterns of asthma mortality in Philadelphia from 1969 to 1991. New England Journal of Medicine 331:1542-1546. Mannino DM, Homa DM, Pertowski CA, Ashizawa A, Nixon LL, Johnson CA, Ball LB, Jack E, Kang DS. 1998. Centers for Disease Control and Prevention. Surveillance for Asthma Prevalence United States, 1960-1995. Morbidity and Mortality Weekly Report. 47(No. SS-1~:1-28. National Academy of Sciences (NAS). 1994. Science and Judgement in Risk Assessment. National Academy Press: Washington, DC. Rappaport S. Boodram B.1998. Forecasted state-specific estimates of self-reported asthma prevalence United States, 1998. Morbidity and Mortality Weekly Report 47~47~:1022-1025.