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5 INDOOR BIOLOGIc Expos u res I he allergic constituents of indoor air are predominantly bio- logic in origin (Becher, 1996~. As early as the sixteenth century, associations between a number of these exposures and asthma were suspected; however, the scientific data available were un- able to confirm such an association. Concern in recent years re- garding the potential health effects of indoor air, as well as the marked increase in the prevalence of asthma in industrialized countries, has prompted an influx of scientific data on exposure to airborne biologic agents and asthma. The committee was charged with the task of evaluating the strength of the scientific evidence concerning the possible asso- ciation between these agents and asthma prevalence and severity. The committee was also tasked with examining possible means of mitigating or preventing exposure to these agents. In this chap- ter the committee evaluates indoor exposure to biologic agents, addressing the following to the extent permitted by available re- search: 1. which factors influence exposures to the agent; 2. whether a relationship exists between the agent and asthma prevalence or severity, taking into account the strength of the sci- entific evidence and the appropriateness of the methods used to detect the relationship; 105

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106 CLEARING THE AIR 3. what type of relationship exists between the agent and asthma; 4. whether there are special considerations regarding the agent (e.g., subpopulations at risk and interactions with other ex- posures); 5. which strategies effectively mitigate or prevent exposure to the agent; 6. whether these strategies only reduce exposures or decrease the occurrence or exacerbation of asthma; and 7. whether these strategies are reasonable for use by the tar- get populations. Each section begins by providing a definition of the agent and a summary of the factors that influence exposure. The evidence concerning the possible association between the agent and asthma is discussed, followed by the committee's conclusions regarding the health impacts. Where information is available, evidence re- garding possible means of mitigating or preventing exposure to the agent is addressed. Each section concludes with any commit- tee recommendations for areas for which additional research is needed with respect to the agent. Because there are great differ- ences in the amount and type of information available on specific agents, the sections vary in their depth and focus. ANIMALS Cats Definition of the Agent and Means of Exposure Cats are kept as pets in 27% of U.S. households. The major cat allergen, Fe! ~ I, is a glycoprotein structured as a heterodimer with two chains of amino acids, which have been defined by poly- merase chain reaction (PCR) and subsequent DNA sequencing (Griffith et al., 1992; Morgenstern et al., 1991; Schou, 1993~. It is found on cat hair and is produced in cat sebaceous, salivary, and anal glands (De Andrade et al., 1996~. In male cats, Fe! ~ I glandu- lar production is under hormonal control and decreases after cas- tration (Zielonka et al., 1994~. As discussed in the Third Interna

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INDOOR BIOLOGIC EXPOSURES 107 tional Workshop report (Platts-MilIs et al., 1997), the clinical sig- nificance of this decrease in allergen production is not certain, since many symptomatic cat-allergic asthmatics in the United States have neutered cats. Further investigation of hormonal and genetic control of Fe! ~ I production could be relevant to the con- tro] of allergen levels in homes with cats. Although 90/O of pa- tients allergic to cats make immunogIobulin E (IgE) to Fe! ~ I (de Groot et al., 1988; Schou, 1993), making Fe! ~ I a marker for the immune response to cat allergens, at least eight other cat aller- gens have been identified (Duffort et al., 1987), suggesting that protection from Fe! ~ I exposure may not be the equivalent of pro- tection from cat allergen exposure. This conclusion is supported by the findings that 66% of the histamine-releasing activity of cat hair and dander extract, and about 60% of the cat dander radioallergosorbent test (RAST) activity, was carried by Fe! ~ I (Schou, 1993~. Touching the cat is only one mode of contact that may result in airborne suspension of allergen and potential direct hand-to- nose deposition of allergen-associated particles. In contrast with cockroach allergen, which is airborne only transiently during the disturbance of household dust, cat allergen can remain airborne for long periods of time, in part because Fe! `1 I is associated to a significant extent with smaller particles of less than 5 ,um (Custovic et al., 1998b). Particles on which cat allergen is carried, coming primarily from cat dander, are also very adherent. Conse- quently cat allergen is spread easily throughout a house, even when cats are kept out of certain rooms. Moreover, cat allergen is easily carried from home to home, office, school, or day care cen- ter by those who touch cats or visit households with cats (Custovic et al., 1998a; Dybendal and Elsayed, 1994; Warner, 1992~. At trace or small amounts that may be significant for sensi- tization or exacerbation of disease in sensitized individuals, Fe! `1 I in settled dust is found in most homes without cats (Bollinger et al., 1996; Chew et al., 1998), although allergen levels are generally higher in homes with cats. A Baltimore, Maryland, study found measurable levels of airborne Fe! ~ I in 37 homes with cats (range, 1.8-578 ng/m3; median, 45.9 ng/m3) and in 10 of 40 homes with- out cats (range for detectable samples, 2.8-88.5 ng/m3; median, 17 ng/m3) (Bollinger et al., 1996~. In 38 of 40 homes without cats,

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108 CLEARING THE AIR Eel d I was present in the settled dust (range, 39-3,750 ng/g; me- dian,258 ng/g); dust levels were weakly correlated with airborne levels. Carpeting, bedding, and upholstered furniture can be res- ervoirs for deposited cat allergen (Wood et al., 1989~; shaking the bedding in rooms with cats resuspends cat allergen in the air. As well as being detected in homes without cats, cat allergen has also been detected in public places such as hospitals and schools. In one British study that measured both settled and air- borne cat allergen in hospitals, the amount of cat allergen in settled dust in upholstered chairs was as high as in homes with cats (geometric mean, 23,ug/g dust), but airborne levels were low (0.22 ng/m3) (Custovic et al., 1998a). Evidence Regarding Asthma Exacerbation In cat-sensitized asthmatics, cat allergen can induce allergic symptoms, asthmatic symptoms, and decrements in lung func- tion. Exposure to inhaled cat allergen in an experimental cat room led to significant decreases in forced expiratory volume in one second (FIVE range, 6-57%; mean, 25%) in a study of 13 adults with cat allergy. The percentage decrease in FEVER did not corre- late significantly with either the intradermal titration end point with cat allergen or the magnitude of the RAST response with cat allergen. Those cat-allergic subjects classified as asthmatic by methacholine challenge testing experienced almost identical re- sponses to environmental allergen challenge in an experimental cat room and inhalation challenge with cat allergen (Sicherer et al., 1997~. Norman and colleagues documented progressive in- creases in both nasal and lung symptom scores during a 60- minute period in a cat room (Norman et al., 1996~. While initial cat room studies involved very high airborne cat allergen levels, a later experimental cat room exposure study by Bollinger and colleagues (1996) evaluated symptom and lung function responses of cat-sensitive subjects to low-level airborne cat allergens. They demonstrated that cat-sensitive individuals can have increases in upper- (congestion, rhinorrhea, pruritus) and lower- (chest tightness, wheezing) respiratory symptoms and decrements in Jung function at levels of cat allergen occurring in

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INDOOR BIOLOGIC EXPOSURES 109 homes without cats. The median FEVER change was 15% in the seven challenges with a Fe! ~ I level less than 100 ng/m3. In a Delaware case-control study, Gelber and colleagues (1993) studied allergen predictors of emergency room visits for asthma. This study compared 93 patients, 15 to 55 years of age, who pre- sented with breathlessness and airway obstruction, to 93 patients presenting without breathlessness. For cat and cockroach, the combination of sensitization and the presence of allergen in the house was associated with asthma presenting to hospitals (14/93 asthmatics versus 1/93 controls). Whether other exposures po- tentiate the response of cat-allergic asthmatics to cat exposure is unknown. In a cross-sectional study of children in New Mexico with asthma or bronchial hyperresponsiveness, cat sensitization and exposure to cat allergen were common (Sporik et al., 1995~. Among children with asthma (defined as symptomatic bronchial reactivity), 13/19 were sensitized to cat. Numbers were too small to compare symptoms in cat-sensitized asthmatics with and with- out significant home exposure to cat allergen (Ingram et al., 1995~. Evidence Regarding Asthma Development Insufficient data are available to assess whether exposure to cats influences the development of asthma. Cross-sectional stud- ies of children suggest an association between sensitization to cats and home exposure in the first six months of life (Suoniemi et al., 1981; Warner et al., 1991~. These studies may be subject to recall bias. A longitudinal birth cohort study from the Isle of Wight found that the presence of a cat in the home predicted a greater risk of skin test reactivity to cat and a greater risk of any skin test reactivity by 2 years of age (Hide et al., 1994~. Sensitization to cat predicts asthma development, but this may simply be a confir- mation of the well-documented fact that atopic individuals are more likely to develop asthma than nonatopic individuals. In a New Zealand birth cohort study, the development of asthma by 13 years of age was associated with sensitization to cats and dogs at age 13 (Sears et al., 1989~. Sensitization to cats predicted the development of bronchial hyperresponsiveness in a longitudinal study of adults in Boston, Massachusetts (Litonjua et al., 1997~. However, neither of these studies provides evidence of whether

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110 CLEARING THE AIR exposure to cats predicts either asthma or bronchial hyperrespon- siveness. Since cat allergen exposure can potentially take place either at home or in schools and public places, the relative impor- tance of home versus community-wide exposure to cat allergen in the risk of specific sensitization to cats is unknown. Although the field of the genetics of asthma is in its infancy, preliminary studies suggest that certain genetic phenotypes are associated with allergy to specific insects or animals (Fukuda et al., 1995; Hizawa et al., 1998; Young et al., 1992, 1993~. Under- standing the genetics of allergy and asthma, including under- standing the phenotypes associated with allergy specificity, may eventually prove useful in understanding gene-by-environment interaction in the development of asthma. Conclusions: Asthma Exacerbation and Development In cat-sensitive asthmatics, cat allergen exposure leads to worsening of respiratory symptoms and to a decline in Jung func- tion. Although sensitization to cats is a prerequisite to reactivity to cat exposure, the level of airborne cat allergen that exacerbates asthma varies by individual and is not necessarily predictable by the size of the skin test reaction to cat or the titer of IgE antibody. However, specific sensitive subgroups have not been defined. The relationship between cat allergen in the home and asthma devel- opment is uncertain. Because cat allergen is frequently found out- side the home and in households without cats, the assessment of individual exposures to cats is difficult, making evaluation of the association between cat allergen exposure and asthma develop- ment difficult as well. In summary: There is sufficient evidence of a causal relationship between cat allergen exposure and exacerbation of asthma in individuals specifically sensitized to cats. There is inadequate or insufficient evidence to determine whether or not an association exists between cat allergen expo- sure and the development of asthma.

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INDOOR BIOLOGIC EXPOSURES Evidence Regarding Exposure Mitigation and Prevention: Homes 111 Removal of the cat from the home will decrease exposure to cat allergen and is widely recommended for symptomatic cat-sen- sitive asthmatics. However even when the owner removes the cat, cat allergen levels may remain elevated for 20 weeks or more (Wood et al., 1989~. Removal of carpets and upholstery, with en- casement of mattresses and pillows, may be required for dimin- ishing cat allergen to levels commonly measured in homes with- out cats (Wood et al., 1989~. No studies are available that evaluate symptoms or Jung func- tion in cat-sensitive asthmatics before and after removal of the cat from the home. Nor are there studies of change in symptoms or lung function after moving from a home with a cat to a home without a cat. However, exposure studies suggest that in cat-sen- sitive subjects the decline in lung function associated with low- leve] airborne exposure to cat allergen, which can be present in a home with no cats, tends to be less extreme than the decline in Jung function associated with higher-level airborne exposure (Bollinger et al., 1996~. The experiments demonstrating entry into a room with a cat as a source of exacerbation of asthma in cat- sensitive individuals also suggest that removal of the cat from the household may decrease symptoms in cat-allergic asthmatic. Because of the reluctance of cat-allergic symptomatic asthmat- ics to get rid of their cats, a number of studies have focused on the potential for lowering cat allergen levels by washing the cat. In eight households with cats, de Blay and colleagues (1991a) found that the combination of washing the cat weekly, reducing furnish- ings, vacuum cleaning, and air filtration reduced airborne cat al- lergen levels. In a second study, however, Avner and colleagues (1997) from the Platts-MilIs group found that while washing cats by immersion will transiently remove significant allergen from the cat and reduce the quantity of airborne Fe! ~ I, this reduction in allergen is not maintained by one week. Klucka and colleagues (1995) found no significant reduction of Fe! ~ I by washing, use of Allerpet-C (a widely advertised topical spray), or acepromazine, a tranquilizer advocated as efficacious in subsedating doses. While removal of the cat from the living room and bedroom areas

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112 CLEARING THE AIR of the home and use of a High-Efficiency Particulate Air (HEPA) filter reduced airborne levels of cat allergen in homes with cats, the reduction was not evenly spread across the particle size range (Custovic et al., 1998b). It is unclear that the level of reduction of allergen obtained in this study is sufficient to influence symp- toms in cat-sensitized asthmatics. No studies are available to as- sess the efficacy of recommendations to wash cats in reducing symptoms in cat allergic-asthmatics. Although the combination of HEPA filter use, mattress and pillow covers, and exclusion of cats from the bedroom reduced airborne cat allergen levels, a Maryland study detected no improvement in daily symptom scores, peak flow rates, medication use, monthly spirometry, pre- and post-study cat-specific IgE levels, and methacholine chal- lenge studies in cat-allergic subjects (Wood et al., 1998~. On the other hand, in a double-blind, placebo-controlled, cross-over study of twenty asthmatic children sensitized to cat or dog aller- gens, and living in homes with these animals, airway hyperresponsiveness was improved and peak flow variation was decreased during the use of air cleaners in the living room and bedroom of the child (van der Heide et al., 1999~. The authors report that substantial amounts of cat and dog allergen were cap- tured by the air cleaners; floor cat and dog allergen levels were unchanged by air cleaner use. Evidence Regarding Exposure Mitigation and Prevention: Schools and Hospitals Even if the cat is removed from the home, continued low- grade exposures may occur in public places or via clothes from cat owners. Since cat allergen is everywhere, there is little poten- tial for absolute avoidance (Dybendal and Elsayed, 1994; Warner, 1992~. Norwegian investigators have demonstrated the presence of Fe! ~ 1 in schools on both smooth and carpeted floors, with approximately 11 times more allergen on the carpeted floors (Dybendal et al., 1991, 1989a, 1989b). The frequency of cleaning floors and furniture was believed to influence the level of cat and dog allergen, which were higher on chairs than in floor dust (Warner, 1992~. Upholstered chairs and mattresses in hospitals are

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INDOOR BIOLOGIC EXPOSURES 113 also demonstrated reservoirs for cat and dog allergen (Custovic et al., 1998a). To lessen the risk of exacerbation of asthma in cat- or dog- sensitized asthmatics in public buildings, Warner and others (1992) have recommended the use of smooth floors and frequently cleaned wooden or plastic chairs. In their study demonstrating the presence of significant cat and dog allergen levels in a hospi- tal in Manchester, England, Custovic and colleagues (1998a) ques- tioned the introduction of soft furnishings and carpets into hospi- tals where highly cat- or dog-allergic asthmatics may come for care. Where upholstered chairs were present, they demonstrated that vacuuming three times a week significantly reduced allergen levels. Conclusions: Exposure Mitigation and Prevention Cat allergen levels can be reduced to levels found in homes without cats by removal of the cat from the home, but the reduc- tion in allergen levels may require a prolonged period of time. The combination of HEPA filter use, mattress and pillow covers, and exclusion of cats from the bedroom may not reduce airborne cat allergen levels sufficiently to improve symptoms in cat-sensi- tive asthmatics. The absence of carpet, the use of plastic or wooden rather than upholstered chairs, and of frequent vacuum- ing in schools and hospitals may decrease the levels of cat aller- gen in public places. No studies are available to evaluate whether these measures improve symptoms or lung function in cat-sensi- tized asthmatics or whether they decrease the potential for sensi- tization in nonsensitized individuals. In summary: There is sufficient evidence of an association between re- moval of a cat from the home and a decrease in levels of cat aller- gen in the home; this decrease in levels of allergen may be slow if reservoirs of cat allergen are not simultaneously removed from the home. 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. There is limited or suggestive evidence of an association

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114 CLEARING THE AIR between measures short of removal of a cat from the home (e.g., washing the cat, HEPA filter use) and some transient reduction in cat allergen levels in the home. 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 (e.g., washing the cat, HEPA filter use) and improvement in symptoms in cat-allergic asthmatics. Dogs Definition of the Agent and Means of Exposure Dogs are present in 31% of U.S. households and are also sources of allergens (Schou, 1993~. Allergy to cats is reported to be about twice as common as allergy to dogs, despite the fact that dogs are as common in U.S. households as cats (Bollinger et al., 1996~. CanfI and CanfII are purified dog allergens that have been identified (Schou, 1993~. CanfIis a polypeptide whose molecular weight and structure have been partially but not fully defined (Schou, 1993~. It is present in dander, pelt, hair, and saliva, but not in the urine or feces of dogs (Schou, 1993~. Though there are likely to be other dog allergens, no others have been found to have clini- cal importance. CanfIis considered a major allergen, because it accounts for at least half of the allergenic activity in dog hair and dander. In addition, 92% of dog-allergic patients had a positive skin prick test to CanfI (Schou, 1993; Yman et al., 1973~. It is still a controversial matter whether true breed-specific dog allergens exist or whether the differences observed between breeds are quantitative rather than qualitative (Schou, 1993~. Hair is not the only source of dog allergen, and it is not known whether short- haired dogs are less allergenic. Cross-reactivity can be found be- tween dog and cat allergen (Vanto and Koivikko, 1983~. Dog allergen, like cat allergen and unlike cockroach, is easily aerosolized and widely disseminated throughout the community (Custovic et al., 1997~. In a Baltimore study of 42 homes, dog anti- gen was demonstrated in more than half of households (Lied et al., 1987; Schou, 1993~. In Sweden, dog allergen has been mea- sured in homes that have never had dogs (Munir et al., 1992~. Like cat allergen, dog allergen has been found in significant

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INDOOR BIOLOGIC EXPOSURES 115 amounts in public buildings such as schools (Berge et al., 1998; Dybendal et al., 1989a; Schou, 1993; Warner, 1992) and hospitals (Custovic et al., 1998a). In dust from upholstered English hospital chairs, CanfI levels (geometric mean = 22,ug/g, range, 4-63) were as high as levels in settled dust from households with dogs (Custovic et al., 1998a; Munir et al., 1994~. Hospital airborne Canf I levels were detectable in 7 of 10 testing days but were lower (range 0.09-0.22 ng/m3) than those often found in homes with dogs (range 0-100 ng/m3 Canf I) (Custovic et al., 1998a; Hodson et al., 1999~. Evidence Regarding Asthma Exacerbation The asthmatic response to bronchial provocation test (PT) with dog allergen was evaluated in a cross-sectional Finnish study of 203 asthmatic children selected from the Children's Asthma Registry (Vanto and Koivikko, 1983~. Of those with a positive PT, 64% had kept dogs, whereas only 36% with a negative PT had kept dogs. A positive PT was correlated with a positive skin prick test to dog (correlation coefficient = 0.8), but not with the fre- quency of reported asthma symptoms. In immunotherapy trials, positive response to bronchial provocation with dog allergen has also been associated with elevated levels of IgE to dog allergen in asthmatic subjects (Hedlin et al., 1995; Valovirta et al., 1984; Vanto et al., 1980~. Some investigators consider symptomatic and bron- chial response to animal allergen in an experimental animal room to be more definitive proof that animal allergen triggers asthma than allergen bronchial PT. They question whether the airway re- sponse to bronchial provocation with an allergen is always an allergic rather than an irritant response. The committee could find no published studies of the response of dog-sensitized asthmatics to exposure to dogs in an experimental dog room analogous to the cat room set up by the Hopkins group (Sicherer et al., 1997~. Evidence Regarding Asthma Development There is insufficient evidence regarding the role of dog aller- gen in the development of asthma. In keeping with the ecology of Los Alamos, New Mexico, which is high and dry, with less dust

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212 CLEARING THE AIR Pugin J. Schurer-Maly CC, Leturcq D, Moriarty A, Ulevitch RJ, Tobias PS. 1993. Lipopolysaccharide activation of human endothelial and epithelial cells is mediated by lipopolysaccharide-binding protein and soluble CD14. Proceedings of the National Academy of Sciences of the United States of America 90~7~:2744-2748. Pullan CR, Hey EN. 1982. Wheezing, asthma, and pulmonary dysfunction 10 years after infection with respiratory syncytial virus in infancy. British Medical Journal (Clinical Research Edition) 284~6330~:1665-1669. Rains N. Siebers R. Crane J. Fitzharris P. 1999. House dust mite allergen (Der p I) accumulation on new synthetic and feather pillows [see comments]. Clinical and Experimental Allergy 29~2~:182-185. Rakes GP, Arruda E, Ingram JM, Hoover GE, Zambrano JC, Hayden FG, Platts- Mills TAE, Heymann PW. 1999. Rhinovirus and respiratory syncytial virus in wheezing children requiring emergency care. American Journal of Respiratory and Critical Care Medicine 159~3~:785-790. Rao CY. 1999. A quantitative risk assessment for Stachybotrys chartarum exposure. D. Sc. Thesis, Department of Environmental Health, Harvard School of Public Health, Boston. 152 pages. Rautalahi M, Terho EO, Vohlonen I, Husman K. 1987. Atopic sensitization of dairy farmers to work-related and common allergens. European Journal of Respiratory Diseases 71 (Supplement 152~:155-164. Rautiala S. Reponen T. Nevalainen A, Husman T. Kalliokoski P. 1998. Control of exposure to airborne viable microorganisms during remediation of moldy buildings; report of three case studies. American Industrial Hygiene Association Journal 59~7~:455-460. Richard JL, Thurston JR. 1975. Effect of aflatoxin on phagocytosis of Aspergillus fumigatus spores by rabbit alveolar macrophages. Applied Microbiology 30~1~:44-47. Richards G. Kolbe J. Fenwick J. Rea H. 1995. The effects of privet exposure on asthma morbidity. New Zealand Medical Journal 108~996~:96-99. Rietschel ET, Brade H. 1992. Bacterial endotoxins. Scientific American 267~2~: 55-61. Robinson D, Hamid Q. Bentley A, Ying S. Kay AB, Durham SR. 1993. Activation of CD4+ T cells, increased TH2-type cytokine mRNA expression, and eosinophil recruitment in bronchoalveolar ravage after allergen inhalation challenge in patients with atopic asthma. Journal of Allergy and Clinical Immunology 92~2~:313-324. Romagnani S. 1992. Human TH1 and TH2 subsets: regulation of differentiation and role in protection and immunopathology. International Archives of Allergy Immunology 98~4~:279-285. Roman M, Calhoun WJ, Hinton KL, Avendano LF, Simon V, Escobar AM, Gaggero A, Diaz PV. 1997. Respiratory syncytial virus infection in infants is associated with predominant Th-2-like response. American Journal of Respiratory and Critical Care Medicine 156~1~:190-195.

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INDOOR BIOLOGIC EXPOSURES 213 Ronmark E, Lundback B. Jonsson E, Platts-Mills T. 1998. Asthma, type-1 allergy and related conditions in 7-and 8-year-old children in northern Sweden: prevalence rates and risk factor pattern. Respiratory Medicine 92~2~:316-324. Rosas I, McCartney HA, Payne RW, Calderon C, Lacey J. Chapela R. Ruiz-Velazco S. 1998. Analysis of the relationships between environmental factors (aeroallergens, air pollution, and weather) and asthma emergency admissions to a hospital in Mexico City. Allergy 53~4~:394-401. Rosenstreich DL, Eggleston P. Kattan M, Baker D, Slavin RG, Gergen P. Mitchell H. McNiff-Mortimer K, Lynn H. Ownby D, Malveaux F. 1997. The role of cockroach allergy and exposure to cockroach allergen in causing morbidity among inner-city children with asthma. New England Journal of Medicine 336~19~:1356-1363. [Comment in N Engl J Med 1997. 336~19~:1382-1384 and 337~11~:791-792.] Rylander R. Haglind P. Lundholm M, Mattsby I, Stenqvist K. 1978. Humidifier fever and endotoxin exposure. Clinical Allergy 8~5~:511-516. Rylander R. Morey P. 1982. Airborne endotoxin in industries processing vegetable fibers. American Industrial Hygiene Association Journal 43~11~:811-812. Saito K, Nishijima M, Ohno N. Nagi N. Yadomae T. Miyazaki T. 1992. Activation of complement and Limulus coagulation system by an alkali-soluble glucan isolated from Omphalia lapidescens and its less branched derivatives. Chemical and Pharmaceutical Bulletin 40:1227-1230. Sakaguchi M, Inouye S. Miyazawa H. Kamimura H. Kimura M, Yamazaki S. 1990a. Evaluation of countermeasures for reduction of mouse airborne allergens. Laboratory Animal Science 40~6~:613-615. Sakaguchi M, Inouye S. Yasueda H. Irie T. Yoshizawa S. Shida T. 1990b. Measurement of allergens associated with dust mite allergy. II. Concentrations of airborne mite allergens (Der I and Der II) in the house. International Archives of Allergy and Applied Immunology 90~2~:190-193. Sakamoto T. Ito K, Yamada M, Iguchi H. Ueda M, Matsuda Y. Torii S. 1990. Allergenicity of the osmophilic fungus Aspergillus restrictus evaluated by skin prick test and radioallergosorbent test [Japanese]. Arerugi Japanese Journal of Allergology 39~11~:1492-1498. Sakurai T. Ohno N. Yadomae T. 1994. Changes in immune mediators in mouse lung produced by administration of soluble (1~3~-beta-D-glucan. Biological and Pharmaceutical Bulletin 17~5~:617-622. Sanchez H. Bush RK. 1994. Complete sequence of a cDNA encoding an Alternaria allergen. Journal of Allergy and Clinical Immunology 93:208 [abstract]. Santiago-Schwarz F. McHugh DM, Fleit HB. 1989. Functional analysis of monocyte-macrophages derived from nonadherent cord blood progenitor cells: correlation with the ontogeny of cell surface proteins. Journal of Leukocyte Biology 46~3~:230-238. Saraf A, Larsson L, Burge H. Milton D. 1997. Quantification of ergosterol and 3- hydroxy fatty acids in settled house dust by gas chromatography mass spectrometry comparison with fungal culture and determination of endotoxin by a Limulus amebocyte lysate assay. Applied and Environmental Microbiology 63:2554-2559.

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