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9 ASTHMA AND NONRESIDENTIAL INDOOR E~viroun~ents M any cross-sectional epidemiologic studies document an association of asthma diagnoses or asthma symptoms with as- pects of the residential environment, such as dampness or mold. In contrast to residences, nonindustrial work buildings often have large numbers of occupants in whom the epidemiology of asthma can be studied in relation to the built environment. Several lines of evidence suggest the efficiency of pursuing indoor environ- mental factors in relation to asthma among office workers, school staff, and students. This chapter briefly reviews the scientific literature regarding asthma and nonresidential indoor environments primarily of- fice buildings and schools. Industrial environments, which may expose workers to a wide variety of allergens and irritants ca- pable of inducing asthma (Chan-Yeung, 1995), are outside the scope of this chapter and report. BUILDING-RELATED ASTHMA New-onset asthma caused by specific building environments has been investigated infrequently. Case reports of office build- ing-related asthma with a clear work-related pattern exist, and the causes were related to humidifiers or the biocides used in hu- midifiers (Finnegan and Pickering, 1986; Robertson and Burge, 316

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ASTHMA AND NONRESIDENTAL INDOOR ENVIRONMENTS 317 1985~. Epidemic asthma occurred in a printing factory in associa- tion with a contaminated humidifier (Burge et al., 1985~. The most compelling description of office building-related asthma found that employees of a county social services agency in Denver had a 2.9-fold rate of physician-diagnosed asthma arising since build- ing occupancy compared to employees of a comparable subur- ban social service agency (Hoffman et al., 1993~. The Denver workers reported excess shortness of breath and chest tightness, and 36% of Denver employees with preexisting asthma reported exacerbation of their asthma in relation to building occupancy, in contrast to none of the preexisting asthma cases in the suburban county agency. Peak expiratory flow measurements of a sentinel case fell markedly over the course of time at work, with recovery within an hour outside the office building. Bronchial reactivity measurements from serial methacholine challenge tests showed improvement to the normal range within two to three months of assignment to another building; recurrence of bronchial hyperre- activity with reassignment to the implicated building; and partial resolution with removal for the second time. In addition to a 4.9- fold excess of asthma with onset or exacerbation since building occupancy, cases of hypersensitivity pneumonitis and other in- terstitial lung disease occurred among occupants of the implicated building. In this investigation, the suspected cause was bioaerosols associated with below-grade moisture incursion from the posterior wall that was built into an earthen bank. Although the few publications discussed above document the phenomenology of building-related asthma, little information ex- ists regarding the contribution of building-related asthma to the increasing asthma burden in the United States or elsewhere. Sev- eral state health departments solicit physician case reports of oc- cupational asthma for the purpose of state- or federally funded surveillance. Data from four states reported to the National Insti- tute for Occupational Safety and Health (NIOSH) for 1993-1995, documented 86 physician-diagnosed cases attributed to indoor air quality deficiencies, without other specific cause, accounting for 8% of all occupational asthma cases recognized by reporting physicians (Romero lajosky et al., l999~. Michigan, Massachusetts, and Connecticut supplied data over a longer time, which docu- ment increasing proportions of all reported occupational asthma

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318 CLEARING THE AIR cases attributable to indoor environmental quality, up to 25% (un- published reports from Carolyn lean Dupuy, Connecticut Depart- ment of Public Health, Respiratory Disease and the Indoor Envi- ronment, sent to NIOSH by emai! on May 13, 1999; from Ruth Vanderwaals, Michigan Department of Public Health sent by emai] on March 22, 1999; and from Letitia Davis, Massachussetts Department of Health, sent by emai] on March 6, 1999~. Another source of physician case reporting is the data base of the Association of Occupational and Environmental Health Clin- ics (AOEC). An unpublished report indicates that from 1991 to 1996, 15% of the 542 occupational asthma cases seen in the report- ing members of largely academic clinics were related to indoor air exposures, with the annual proportion increasing from 6% in 1991 to 30/O in 1996 (Hunting, 1999~. Half of the cases of reported asthma-reactive airways dysfunction syndrome (RADS) from pri- mary and secondary schools and vocational schools in this data base were attributed to indoor air exposures. These data must be interpreted with caution because the number and location of re- porting clinics varied from year to year and the numbers are likely influenced by the characteristics of the responding facilities. This limited information from practitioners reporting to pub- lic health agencies or their occupational health association sug- gests that physicians are seeing patients with work-related pat- terns of asthma symptoms or objective measurements for which they are unable to identify specific causes apart from alleged poor indoor air quality. Investigations in response to these reports by public health agencies have been limited by lack of knowledge about what agents to measure in evaluating hazards for asthma or for less specific indoor air quality (IAQ) complaints. Attribution of asthma and asthma symptoms to specific build- ing environments by the lay public far exceeds physician recogni- tion of building-related asthma. One source of data regarding public concerns about building contributions to asthma are the requests from employees or management for Health Hazard Evaluations, a mandated service program of NIOSH. Since the late 1970s, after the energy crisis and changes in ventilation codes, health hazard evaluations coded as "indoor air quality requests" from office and school employees have increased persistently in numbers and proportions of all requests. Of the 100-200 IAQ re

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ASTHMA AND NONRESIDENTAL INDOOR ENVIRONMENTS 319 quests received each year since 1990, the proportion mentioning asthma in the written request increased during the 1990s to 14% in 1998; the proportion mentioning any chest symptom increased to 46% in 1997-98. Among IAQ requests mentioning asthma as a health concern to be investigated in the health hazard evaluation, a substantial minority 43% come from school staff, manage- ment, or unions representing teachers. Most office workers do not attribute chest symptoms to their building environments. Preliminary analyses of questionnaire in- formation from occupants of 29 buildings surveyed in the U.S. Environmental Protection Agency's (EPA's) Building Assessment and Evaluation Study (Brightman et al., 1997), revealed that the median prevalence of occupants reporting frequent work-related shortness of breath was 2%. An unpublished NIOSH report evalu- ating a series of buildings selected without regard to indoor air quality complaints indicated a maximum prevalence of 8% (Sieber and Godwin, 1998~. In contrast, one-third of 80 office buildings studied by NIOSH in 1993 in response to health hazard evalua- tion requests had prevalences of frequent work-related shortness of breath greater than 8%, ranging up to 24% (Malkin et al., 1996~. In conclusion, most buildings in which occupants have IAQ com- plaints probably do not have excesses of respiratory disease, but a substantial subset of "complaint" buildings may have occupants who associate their chest symptoms with building occupancy. The NIOSH experience with indoor air quality investigations in 1993 gives some epidemiologic leads regarding building-re- lated asthma and its causes (Sieber et al., 1996~. Among 2,435 OC- cupants of 80 office buildings classified according to whether moisture was found in the heating, ventilation, and air-condition- ing (HVAC) system, the prevalence of physician-diagnosed asthma arising since building occupancy was 61% higher in build- ings with HVAC moisture, and the prevalence was doubled of having three of four chest symptoms (cough, shortness of breath, wheezing, and chest tightness) at least once per week in the last month that improved away from work (Table 9-1~. In logistic analyses controlled for age and gender, postoccupancy asthma was associated with dirty HVAC filters, debris in the air intake system, and renovation with drywall within the previous three weeks; daily surface cleaning with wet methods appeared protec

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320 CLEARING THE AIR TABLE 9-1 Health Conclition Prevalence (%), by Moisture Status of HVAC Among 2,435 Occupants of DO Office Builclings with IAN Complaints Moisture Moisture Health Condition Present Absent Range Any physician-diagnosed asthma 11.7 11.6 Postoccupancy asthma 3.7 2.3 0-33.3 Chest symptomsa 4.1 1.8 0-33.3 aThree of four (cough, shortness of breath, wheezing, chest tightness) occurring >1/week in last month and improving away from work. SOURCE: W. Karl Sieber, Division of Surveillance, Hazard Evaluations, and Field Studies, National Institute for Occupational Safety and Health, written communication to Kathleen Kreiss, March 8,1999. TABLE 9-2 Relative Risks by Health Conclition for Environmental Factors Environmental Variable Postoccupancy Asthma Multiple Chest Symptoms Dirty filters 2.0 a 1.9 a Air intake debris 2.0 a 3.1 a Recent renovation with drywall 2.5 a 1.1 Ceiling panels 3.2 3.4 Daily surface cleaning 0.5 a 0.7 apt< .05. SOURCE: W. Karl Sieber, Division of Surveillance, Hazard Evaluations, and Field Studies, National Institute for Occupational Safety and Health, written communication to Kathleen Kreiss, March 8,1999. five in logistic regression models (Table 9-2~. Similar risk factors existed for the outcome of frequent multiple work-related chest symptoms, which may represent asthma-like conditions for which medical consultation has not been sought or for which an asthma diagnosis was not made. Although these findings do not

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ASTHMA AND NONRESIDENTAL INDOOR ENVIRONMENTS 321 document specific agents causing asthma in office buildings, they suggest that bioaerosols associated with HVAC moisture, mainte- nance deficiencies, and water damage requiring renovation are promising hypotheses. Commercial office building stock and schools are often con- structed with flat roofs, which predispose to puddling and mois- ture incursion; other common sources of moisture problems in nonindustrial building stock are HVAC coils, drain pans, and duct liners; below-grade drainage; inadequate moisture barriers; flash- ing leaks; flooding; and plumbing mishaps. At present, little in- formation is available regarding the relative health risks of these conditions. Absent risk assessment information, building occu- pants, tenants, and managers have little leverage to have these conditions fixed. STUDIES OF SCHOOLS School is an important indoor environment for many children. The possible influence on health of indoor air in schools and day care centers have been the subject of research. However, very little of this literature specifically addresses indoor air exposures and asthma. Of the available studies on the topic, few have done care- ful and complete exposure assessments. Schools are subject to many of the same exposure problems found in homes, although not necessarily at the same levels. The level of some allergens such as cockroach and dust mite is thought to be generally lower in schools because of the relative scarcity of appropriate habitats for infestation (Perzanowski et al., 1999; Sarpong et al., 1997~. The absence of a direct source does not, how- ever, necessarily preclude its presence. Cat allergen which clings to clothing and other belongings has been measured in schools and other indoor environments where cats have never been (Chan-Yeung et al., 1999~. Indeed, schools may be a major source of exposure to cat and dog allergen for individuals who do not have these pets at home (Almqvist et al., 1999; Lonnkvist et al., 1999~. A survey of research on indoor air quality in schools noted that the major building-related problem identified was inad- equate outdoor air ventilation (Daisey and Angell, 1998~. Water

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322 CLEARING THE AIR damage and concomitant mold growth constituted the second greatest problem. Among the epidemiologic studies identified by the commit- tee, Smoke and colleagues (1997) investigated air quality, envi- ronmental characteristics, and asthma outcomes in 762 students in 39 schools in Uppsala County, Sweden. They used a self-ad- ministered questionnaire for health status information and em- ployed trained occupational hygienists to gather building infor- mation and measurements in the schools. Data gathered included air exchange rate, temperature, and relative humidity; airborne levels of volatile organic compounds (VOCs), NO2, molds, and bacteria; and levels of endotoxin, and cat, dog and mite allergen in settled dust. They found that self-reported current asthma was more common in schools that were larger, and had more open shelves (a repository of settled dust), lower room temperature, higher relative humidity, higher concentrations of formaldehyde or other VOCs, viable mold or bacteria, and more cat allergen. The observations were drawn on the basis of 40 asthma cases. Haverinen and colleagues (1999) investigated three school buildings that were suspected of causing occupant health prob- lems. The buildings were subjected to extensive structural and microbial contamination surveys; questionnaires were used to collect data on health problems. Widespread moisture damage was observed. Fungi identified (Aspergillus, Eurotium) were typi- cal of buildings with mold problems. The prevalence of self-iden- tified asthma among upper secondary school students, but not elementary or high school students, was reported to be higher than typical for the age group. Hunting (1999) noted that half (14 of 28) of the cases of re- ported "occupational asthma" or RADS from primary and sec- ondary schools and vocational schools in AOEC's Occupational and Environmental Disease Surveillance Database over the years 1991-1996 were attributed to indoor air exposures. The specific exposures were not identified. Nafsted and colleagues (1999) investigated the respiratory health of 3,853 children in Oslo, Norway. Parents completed a questionnaire concerning day care arrangements, the child's health, environmental conditions, and family characteristics. The study found that the lifetime risk of doctor-diagnosed asthma was

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ASTHMA AND NONRESIDENTAL INDOOR ENVIRONMENTS 323 higher in children who started attending day care centers during the first two years of life. The authors speculated that this was a consequence of the higher rate of early respiratory infections in children in day care. There were no data reported on other envi- ronmental exposures. Two studies addressed respiratory outcomes in children in the United States. A study of 1,268 children in Minnesota by Marbury and colleagues (1997) found that day care attendance was associated with an increased risk of recurrent wheezing ill- nesses and lower-respiratory infections. Celedon and colleagues (1999) examined respiratory tract illnesses in 498 Boston-area chil- dren who had at least one parent with a history of allergy or asthma. Researchers found that day care attendance increased the risk of upper and lower respiratory tract illnesses in the first year of life for these children. (Chapter 5 includes a discussion of the state of the literature regarding exposure to infectious agents and asthma.) Such findings are not, however, uniform. McCutcheon and Woodward (1996) studied the respiratory health of 445 Adelaide, South Australia, school children, using data from questionnaires completed by parents and school records. They found that chil- dren who had attended child care prior to commencing school experienced half as many episodes of asthma as children who had never attended child care. Among the explanations for the findings offered was protection against later respiratory illness as a result of early exposure, although selection of ilIness-prone chil- dren into home care might also have had an influence. School exposures are an area of continuing research interest. One ongoing study of schools in the Chicago area is monitoring levels of a wide variety of potentially problematic agents includ- ing molds, dust mites, animal and insect allergens, particulates and various chemicals and other environmental characteristics such as ventilation and humidity. The study is also evaluating the effect of interventions including educational initiatives and inte- grated pest management. An interesting observation from this ef- fort is the importance of involving engineering and janitorial staff, along with school management, in the planning and implementa- tion of interventions (Persky, 1999~.

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324 CLEARING THE AIR CONCLUSION Published case reports, public health surveillance of physi- cian reporting, and cross-sectional studies of building occupants with indoor air quality complaints provide limited or suggestive evidence of an association between aspects of the nonindustrial indoor environment and the development of asthma with a build- ing occupancy-related pattern of symptoms and, in some in- stances, objective abnormalities. What is lacking for the most part, however, is knowledge of specific etiologic agents in these nonin- dustrial indoor environments that might be responsible for these new work-related asthma cases. Epidemiologic data suggest that moisture and ventilation system problems are markers for the problematic agents when work-related asthma arises in particu- lar office and school buildings. Similarly, one cross-sectional study comparing two building populations (with comparable IAQ dis- comfort complaints) provides evidence that one particular office environment caused exacerbation of asthma among more than a third of occupants with preoccupancy physician diagnoses of asthma, and the other office environment did not. However, the proportion of building environments that precipitate exacerba- tion of asthma and the specific etiologies of asthma exacerbation are unstudied. RES"RCH NEEDS The few available studies suggest the importance of building factors in relation to asthma, but further research is critical to as- sessing the attributable risks, remediable risk factors, and means of hazard assessment. Development of methods for representa- tive quantitative assessment of bioaerosols of fungal and bacte- rial origin is a high priority for health outcome studies and haz- ard assessment. In addition, knowledge of the epidemiology of building-related asthma in problem buildings where there are ex- cess chest complaints among occupants, in comparison to build- ings where there are no complaints, can advance our understand- ing of specific bioaerosols in relation to asthma. Research should focus on exposure-response studies of many building environ- ments and populations; clinical investigation of patients with

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ASTHMA AND NONRESIDENTAL INDOOR ENVIRONMENTS 325 building-related asthma; and intervention studies, even without knowing the specific etiology involved. This research agenda re- quires new partnerships among academic investigators, clini- cians, public health agencies, industrial hygienists, and building scientists. REFERENCES Almqvist C, Larsson PH, Egmar AC, Hedren M, Malmberg P. Wickman M. 1999. School as a risk environment for children allergic to cats and a site for transfer of cat allergen to homes. Journal of Allergy and Clinical Immunology 103(6):1012-1017. Brightman HS, Womble SE, Girman JR, Sieber WK, McCarthy IF, Buck RJ, Spengler ID. 1997. Preliminary comparison of questionnaire data from two IAQ studies: occupant and workspace characteristics of randomly selected buildings and "complaint" buildings. Healthy Buildings/IAQ Conference proceedings, September 1997, Washington, DC. Burge PS, Finnegan M, Horsfield N. Emery D, Austwick P. Davies PS, Pickering CA. 1985. Occupational asthma in a factory with a contaminated humidifier. Thorax 40~4~:248-254. Celedon JC, Litonjua AA, Weiss ST, Gold DR. 1999. Day care attendance in the first year of life and illnesses of the upper and lower respiratory tract in children with a familial history of atopy. Pediatrics 104~3 Pt 1~:495-500. Chan-Yeung M. 1995. Occupational asthma. Environmental Health Perspectives 103(Supplement 6~: 249-252. Chan-Yeung M, McClean PA, Sandell PR, Slutsky AS, Zamel N. 1999. Sensitization to cat without direct exposure to cats. Clinical and Experimental Allergy 29(6):762-765. Daisey JM, Angell WJ. 1998. A Survey and Critical Review of the Literature on Indoor Air Quality, Ventilation and Health Symptoms in Schools. Lawrence Berkeley National Laboratory. LBNL-41517. Finnegan MJ, Pickering CAC. 1986. Building-related illness. Clinical Allergy 16~5~:389-405. Haverinen U. Husman T. Toivola M, Suonketo J. Pentti M, Lindberg R. Leinonen J. Hyvarinen A, Meklin T. Nevalainen A. 1999. An approach to management of critical indoor air problems in school buildings. Environmental Health Perspectives 107(Suppl 3~:509-514. Hoffman RE, Wood RC, Kreiss K. 1993. Building-related asthma in Denver office workers. American Journal of Public Health 83~1~:89-93. Hunting K. 1999. Reporting Trends in ASTHMA and RADS Related to Indoor Air Problems. Data from the AOEC Database. [unpublished report dated 3/18/993.

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326 CLEARING THE AIR Lonnkvist K, Hallden G. Dahlen SE, Enander I, van Hage-Hamsten M, Kumlin M, Hedlin G. 1999. Markers of inflammation and bronchial reactivity in children with asthma, exposed to animal dander in school dust. Pediatric Allergy and Immunology 10(1):45-52. Malkin R. Wilcox T. Sieber WK. 1996. The National Institute for Occupational Safety and Health indoor environmental evaluation experience. Part two: symptom prevalence. Applied Occupational and Environmental Hygiene 11(6):540-545. Marbury MC, Maldonado G. Wailer L. 1997. Lower respiratory illness, recurrent wheezing, and day care attendance. American Journal of Respiratory and Critical Care Medicine 155(1):156-161. McCutcheon H. Woodward A. 1996. Acute respiratory illness in the first year of primary school related to previous attendance at child care. Australian and New Zealand Journal of Public Health 20~1~:49-53. Nafstad P. Hagen JA, Die L, Magnus P. Jaakkola JJ. 1999. Day care centers and respiratory health. Pediatrics 103(4 Pt 1):753-758. Persky VW. 1999. Asthma and Exposure in the School Environment. Presentation made at a public workshop before the Committee on the Assessment of Asthma and Indoor Air on March 22, 1999. Washington DC. Perzanowski MS, Ronmark E, Nold B. Lundback B. Platts-Mills TA. 1999. Relevance of allergens from cats and dogs to asthma in the northernmost province of Sweden: schools as a major site of exposure. Journal of Allergy and Clinical Immunology 103~6~:1018-1024. Robertson AS, Burge PS. 1985. Building sickness. Practitioner 229(1404):531-534. Romero Jajosky RA, Harrison R. Reinisch F. Flattery J. Chan J. Tumpowsky C, Davis L, Reilly MJ, Rosenman KD, Kalinowski D, Stanbury M, Schill DP, Wood J. 1999. Surveillance of work-related asthma in selected U.S. states using surveillance guidelines for state health departments California, Massachusetts, Michigan, and New Jersey, 1993-1995. Morbidity and Mortality Weekly Report 48(SS03):1-20. Sarpong SB, Wood RA, Karrrison T. Eggleston PA. 1997. Cockroach allergen (Bla g 1) in school dust. Journal of Allergy and Clinical Immunology 99(4):486- 492. Sieber WK, Stayner LT, Malkin R. Petersen MR, Mendell MJ, Wallingford KM, Crandall MS, Wilcox TG, Reed L. 1996. The National Institute for Occupational Safety and Health indoor environmental evaluation experience. Part three: associations between environmental factors and self-reported health conditions. Applied Occupational and Environmental Hygiene 11~12~:1387- 1392. Sieber WK, Godwin KJ. 1998. Comparison of Prevalence of Medical Symptoms in Two Indoor Environmental Quality (IEQ) Surveys, 1998. Unpublished report of the National Institute for Occupational Safety and Health. Smedje G. Norback D, Edling C. 1997. Asthma among secondary schoolchildren in relation to the school environment. Clinical and Experimental Allergy 29(6):762-765.