fungi are part of the normal environment but exposure levels much 
  over normal may occur indoors in buildings 
 with humidity problems , either due to climate or due to local 
 water damage [ 1 , 2 ] . several studies have reported that 
 children   living in damp and moldy dwellings have a 
 larger prevalence of respiratory symptoms , such as cough , phlegm , 
 wheeze , sore throat and runny nose , as well   as asthma [ 3 , 
 4 ] . there are however only 
 limited data demonstrating dose relationships between mold 
 exposure and the extent of symptoms or clinical markers of 
 inflammation or asthma . in one field study a relation was reported 
 between the extent of upper respiratory symptoms and the exposure 
 to molds , expressed as the amount of airborne 
 ( 1  3)--d - glucan . taiwan is located in a subtropical region with optimal 
 environmental characteristics , such as high temperature and 
 relative humidity that sustain the growth of molds and indoor 
 aeroallergens . our previous work demonstrated that 65% of 
 childrens ' mattresses in taiwan 's homes had der p1 
 allergen levels higher than that 2  g / g , a critical level 
  suggested for atopic 
 sensitization [ 6 , 7 ] . in this study , we measured the number of airborne , viable fungi 
 and house dust mite ( hdm ) allergen levels in the homes of a group 
 of asthmatic children . blood samples were drawn and the amounts of 
 total and specific serum ige were determined . the association 
 between the number of fungal colonies , dust mite allergen 
 exposure , and specific and total ige was evaluated . a randomly selected subgroup of asthmatic children was chosen 
 from our previous environmental survey of domestic exposures to 
 dust mite allergens and airborne fungi in a metropolitan city of 
 southern taiwan . a total of 28 subjects , aged 1012 
 years , were invited through phone contact for clinical 
 confirmation conducted by participating pediatricians for their 
 asthmatic status and blood samples were drawn . the clinical visits 
 took place in winter ( december , january , and february ) at the same 
 time as the environmental measurements . airborne fungal concentrations were measured in the subject 's 
 bedroom once a month during the season . duplicate samples of 
 airborne fungi were collected using burkard sampler , a 
 single - stage hole - to - agar impactor with 100 holes ( model pasa / b , 
 burkard mfg co , rickmansworth , uk ) with malt extract agar 
 plates ( mea ) at a flow rate of 10  lpm . after field sampling , 
 the plates were incubated at 25c for 5 days . the yields of colonies were corrected by using positive - hole 
 conversion table before the calculation of final concentrations , 
 colony forming unit per cubic meter ( cfu / m ) . the average 
 concentrations of monthly measurements ( december , january , and 
 february ) were used to express the airborne fungal exposure 
 levels . dust samples from the child 's mattress were collected by a 
 hand - held vacuum cleaner ( national mc 33000 ) with a glass fiber 
 filter and collected concurrently along the airborne samples . samples were collected by vacuuming for 3 minutes on 1  m 
 of the study area . after the sampling , the samples were sealed 
 with parafilm and stored at 4c before handling . samples were in bbs - t ( 0.1% tween 20 in borate 
 buffer saline , ph 8.0 ) and extracted in the ultrasonic vibrator 
 for 2 hours at 25c . der p1 was measured by 
 two - side , monoclonal - antibody - based elisa . the allergen 
 concentrations were expressed in g of measured allergen per 
 gram of dust and the average concentrations of monthly 
 measurements were used to quantify the der p1 exposures . total serum ige and specific ige antibodies to 
 dermatophagoides pteronyssinus , cladosporium herbarum , 
 and aspergillus fumigatus were measured by a quantitative 
 fluoroimmunoassay ( cap - feia ; parmacia up&john , sweden , 
 detection limit 0.35  ku / l for total ige and specific ige ) . the 
 standard curve was examined in triplicate samples and within the 
 range of 10% of coefficient of variation . a randomly selected subgroup of asthmatic children was chosen 
 from our previous environmental survey of domestic exposures to 
 dust mite allergens and airborne fungi in a metropolitan city of 
 southern taiwan . a total of 28 subjects , aged 1012 
 years , were invited through phone contact for clinical 
 confirmation conducted by participating pediatricians for their 
 asthmatic status and blood samples were drawn . the clinical visits 
 took place in winter ( december , january , and february ) at the same 
 time as the environmental measurements . airborne fungal concentrations were measured in the subject 's 
 bedroom once a month during the season . duplicate samples of 
 airborne fungi were collected using burkard sampler , a 
 single - stage hole - to - agar impactor with 100 holes ( model pasa / b , 
 burkard mfg co , rickmansworth , uk ) with malt extract agar 
 plates ( mea ) at a flow rate of 10  lpm . the yields of colonies were corrected by using positive - hole 
 conversion table before the calculation of final concentrations , 
 colony forming unit per cubic meter ( cfu / m ) . the average 
 concentrations of monthly measurements ( december , january , and 
 february ) were used to express the airborne fungal exposure 
 levels . dust samples from the child 's mattress were collected by a 
 hand - held vacuum cleaner ( national mc 33000 ) with a glass fiber 
 filter and collected concurrently along the airborne samples . samples were collected by vacuuming for 3 minutes on 1  m 
 of the study area . after the sampling , the samples were sealed 
 with parafilm and stored at 4c before handling . samples were in bbs - t ( 0.1% tween 20 in borate 
 buffer saline , ph 8.0 ) and extracted in the ultrasonic vibrator 
 for 2 hours at 25c . der p1 was measured by 
 two - side , monoclonal - antibody - based elisa . the allergen 
 concentrations were expressed in g of measured allergen per 
 gram of dust and the average concentrations of monthly 
 measurements were used to quantify the der p1 exposures . total serum ige and specific ige antibodies to 
 dermatophagoides pteronyssinus , cladosporium herbarum , 
 and aspergillus fumigatus were measured by a quantitative 
 fluoroimmunoassay ( cap - feia ; parmacia up&john , sweden , 
 detection limit 0.35  ku / l for total ige and specific ige ) . the 
 standard curve was examined in triplicate samples and within the 
 range of 10% of coefficient of variation . children were 
 considered as sensitized if the ige concentrations exceeded 
 0.35  ku / l . the number of viable airborne fungi was high ( medium : 19359 , 
 25th75th quartile : 15 35024 525  cfu / m ) in those 
 investigated houses . the predominant indoor genera were 
 cladosporium , aspergillus , penicillium , alternaria , nonsporulating fungi and yeast . cladosporium accounted for almost 85% of the colonies 
 from all indoor samples and was present in high amounts 
 ( 17 691  cfu / m ) . der p1 concentrations on 
 child 's mattress exceeding 2  g / g were found in 78.6% 
 of the houses . the average concentration of der p1 was 
 6.72  g / g ( table 1 ) . no significant relationship was found between 
 levels of der p1 and viable fungi ( r = 0.13 ) . among the 28 children , 23 one 
 child was sensitiz to c herbarum allergen , and two to 
 a fumigatus extract ; all three of them were also 
 hdm - sensitiz . total serum ige levels ranged from 18.8 to 
 2000.0  ku / l , and the average concentration was 772.3  ku / l . as illustrated in figure 1 , there was a positive and 
 significant correlation between the number of airborne fungi and 
 the amount of total ige ( r = 0.4399 and p = .0249 ) ; yet , such a 
 relationship could not be detected between der p1 levels 

 and total ige . study subjects were grouped by the median of viable 
 fungi and der p1 concentrations , respectively . logistic 
 regression identified that the only significant relationship was 
 between the dichotomized level of viable fungi and ige with or = 
 5.06 ( 95% ci : 1.0230.06 ) in univariant analysis . moreover , an 
 increased or of 6.67 ( 95% ci : 1.1955.16 ) between the exposure 
  the ige levels , was found when the 
 exposures to airborne fungi and dust der p1 were 
 concurrently examined in a multivariate analysis . although the sample size was relatively small in this pilot 
 investigation , the sample was selected randomly from the general 
 asthmatic population in the study city . therefore , these results 
 still may reflect the real phenomenon of asthmatic population in 
 this region . the major finding in the study was the relation between the number 
 of viable fungi and the total amount of ige in serum . similar 
 findings are reported from a study conducted in a 
 mold - contaminated school building where elevated ige levels were 
 significantly more common among children in mold - contaminated 
 buildings . another study was performed on persons living 
 in houses with mold problems , using the mold cell wall agent 
 ( 1  3)--d - glucan as a marker for mold cell 
 biomass . total ige levels were dose - related to the amount of 
 ( 1  3)--d - glucan in the homes , independent of 
 atopic sensitization ( beijer et al , personal communication ) . the presence of a relation between mold exposure and total ige 
 increase and the very low prevalence of sensitization to mold 
 among the children studied suggests that a major effect of mold 
 exposure is a general stimulation of the ige production without 
 specific sensitization . an increased level of total ige on the 
 other hand implies a larger risk for sensitization to other 
 agents , as evidenced by the high prevalence of sensitization to 
 hdm . more than 80% of the 28 children were sensitized to 
 d pteronyssinus . this rate is similar to that of the 
 d pteronyssinus sensitization pattern reported from 
 uk and other countries [ 10 , 11 ] 
  but higher than that found in 
 school - age children in taipei , taiwan ( 52% ) . it can be 
 hypothesized that the exposure to mold in that group was lower than 
 that in the houses of the children studied here . data from previous studies on the effects of inhaled 
 ( 1  3)--d - glucan suggest that this agent has 
 the capacity to trigger a th2-like cytokine secretary pattern 
 [ 13 , 14 ] . it is also likely that 
 ( 1  3)--d - glucan , though not an 
 inflammagenic agent in itself , increases the sensitivity to other 
 inflammagenic agents . if these reaction patterns are correct , a 
 primary reason for the asthmatic status among the children could 
 be the exposure to molds . on the other hand , the home environment 
 contains a variety of other microbial agents such as endotoxin 
 and muramic acid . there are thus several agents in the indoor air 
 environment that could explain the presence of an inflammatory 
 response among the exposed children . in summary , a dose - response relationship was demonstrated between 
 the exposure to viable , airborne molds and the amount of total 
 ige and risk was increased as children were under the coexposure 
 to viable fungi and hdm . this suggests that exposure to molds 
 causes an increased sensitivity to other antigens in general and 
 possibly also increases the sensitivity to inflammagenic agents .
we measured the number of airborne , viable fungi and house dust 
 mite ( hdm ) allergen levels in the homes of a group of asthmatic 
 children . 
 blood samples were drawn and the amounts of total and 
 specific serum ige were determined . 
 the association between the 
 number of fungal colonies , dust mite allergen exposure , and 
 specific and total ige was evaluated . 
 the number of viable 
 airborne fungi was high ( 20 543  cfu / m3 ) in those 
 investigated houses . 
 der p1 concentrations on child 's 
 mattress exceeding 2  g / g were found in 78.6% of the 
 houses . 
 a quantitative dose - response relationship was demonstrated 
 between the exposure to viable , airborne molds and the amount of 
 total ige ( r = 0.4399 and p = .0249 ) and the level was further 
 increased in children with coexposure to viable fungi and hdm .