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Quantification of airborne moulds in the homes ofchildren with and without wheeze

David P Strachan, Brian Flannigan, Eileen M McCabe, Frances McGarry

Thorax 1990;45:382-387

AbstractA population survey of 1000 7 year oldchildren found a significant excess ofwheeze among children whose homeswere reported to be mouldy (odds ratio3 70, 95% confidence limits 2-22, 6-15).The airborne mould flora was quantifiedby repeated volumetric sampling duringthe winter in three rooms of the homesof 88 children. All of these had pre-viously completed spirometric testsbefore and after a six minute free run-ning exercise challenge. Total airbornemould counts varied from 0 to 41 000colony forming units (CFU)/m3, butwere generally in the range 50-1500CFU/m3, much lower than the concen-trations found outdoors in summer. Theprincipal types of fungi identified are allknown to be common out of doors, andmost were found on at least one occasionin most of the homes. Median and geo-metric mean total mould counts werenot related to reports of visible mould inthe home, or to a history of wheeze in theindex child. The heterogeneous group ofnon-sporing fungi (mycelia sterilia)were the only airborne fungi present atsignificantly higher concentrations inthe homes of wheezy children (geometricmean 2-1 v 0 7 CFU/m3. A non-significantincrease in total mould counts was ob-served in the homes of children with a10% or greater decline in FEV, afterexercise (geometric mean 354 v 253 CFU/mi3). Questionnaire reports of mould inthe home may be a poor indicator ofexposure to airborne spores. The totalburden of inhaled mould spores fromindoor sources is probably not an impor-tant determinant of wheeze among chil-dren in the general population. Althoughthe association with mycelia steriliacould be a chance finding, these non-sporing isolates may include a potentsource of allergen.

The possibility that fungal spores normallypresent in outdoor air might have a causal rolein asthma and hay fever was first proposedbefore the second world war and becamewidely accepted in the 1950s.12 A review in1981, however, pointed out that much of theevidence was anecdotal and published reportswere inadequate and controversial.3 Type 1cutaneous hypersensitivity reactions to mouldextracts provide the best evidence of a causal

link, but many asthmatic patients who havecutaneous hypersensitivity to fungi are alsoallergic to pollen or house dust mites,24 SO theindependent contribution of mould exposureto their symptoms may be difficult to deter-mine. In a detailed longitudinal study of eightDutch asthmatic subjects known to be allergicto moulds pulmonary complaints were morecommon when outdoor mould spore concen-trations were high, but no association wasfound with indoor concentrations.5

Evidence of an association between asthmaand indoor exposure to mould comes from acase-control study of 72 adults-,with asthmaand 72 age and sex matched control subjects.6Nineteen cases and nine controls reportedvisible mould on the walls of their homes, andthere was a significantly higher prevalence ofpositive radio allergosorbent test (RAST) re-sponses to Penicillium among patients report-ing mould in their homes. These and otherresults' suggest that domestic mould sporesmay be capable of invoking species specifictype 1 hypersensitivity in a small proportionof asthmatic adults.A recent cross sectional study of children

and their parents in selected areas of Glasgow,Edinburgh, and London8 found no associationbetween reports of mould in the home andwheeze among adult respondents. A strongrelation, however, was found between re-ported mould growth and wheeze in children,and total airborne mould spore counts werehigher in the homes of wheezy children. Asurvey of a random sample of 7 year oldchildren in Edinburgh9 found that theprevalence of wheeze was three times greateramong children from homes reported to havevisible mould growth than among childrenfrom allegedly non-mouldy homes. This con-firmed earlier findings in the north west of thecity.1'° Reporting of symptoms was validatedby measuring exercise induced bronchocon-striction in the children. Much of the associa-tion between mould and wheeze could beattributed to biased case ascertainment, butthere were nevertheless more children withexercise induced bronchoconstriction amongthe group from mouldly homes.9The reporting of visible mould in the home

may differ between asthmatic and non-asthmatic individuals, owing to a tendency forasthmatic patients (or their parents) to seek anidentifiable cause for the complaint in theirhome environment. In the Edinburgh study9the possibility of differential reporting ofhousing conditions was initially evaluated bymeasurements of temperature and relative

Department ofEpidemiology andPopulation Sciences,London School ofHygiene and TropicalMedicine, LondonD P StrachanDepartment ofBiological Sciences,Heriot-WattUniversity, EdinburghB FlanniganE M McCabeF McGarryAddress for reprint requests:Dr D P Strachan,Department of HealthSciences, St George'sHospital Medical School,London SW1 7 ORE.Accepted 18 January 1990

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Quantification of airborne moulds in the homes of children with and without wheeze

humidity in the child's bedroom. No differ-ences were found between the bedroom con-ditions of children with and without wheeze. 12Ambient humidity may be a poor indicator ofconditions in specific indoor microenviron-ments, where penetrating moisture or conden-sation on to cold surfaces promotes thegrowth of moulds.'3 The study was thereforeextended to measure exposure to airbornemould spores among children with and with-out wheeze. We postulated that, if substantialreporting bias had occurred, the reports ofmould growth by parents of wheezy childrenwould be associated with lower levels ofmeasured exposure than similar reports byparents of unaffected children.

MethodsPOPULATION SURVEYThe original questionnaire survey and medicalexaminations have been described elsewhere.9Briefly, a random sample of children in theirthird primary year (age 6 '/2 to 7 1/2 in September1986) were chosen. Parents were asked tocomplete a postal questionnaire that inquiredabout recent respiratory symptoms experi-enced by the child and conditions in the home,with particular reference to dampness andvisible mould growth. The study receivedethical approval from the Lothian HealthBoard and Lothian Regional Council depart-ment of education.With parental consent, children were exam-

ined by one author (DPS) at school during thefirst half of 1987, using the American ThoracicSociety protocol." A "Compact" pneumo-tachograph (Vitalograph Ltd, Buckingham)was used to record forced expiratory spiro-grams before and after a six minute free run-ning exercise challenge. The minimum of twosatisfactory recordings of forced expiratoryvolume in one second (FEVy) taken five and 10minutes after exercise was compared with thepre-exercise recording. Bronchial lability wasdefined as the difference between the post-exercise and pre-exercise FEV, divided by thepre-exercise FEVI.At the conclusion of the mycological survey

in March 1988 the parents of each child wereasked to complete a short questionnaire relat-ing to respiratory symptoms during theprevious year. No further measurements ofventilatory function or bronchial lability weremade.

SELECTION OF HOMESOne third of the childien in the main surveywere selected for continuous measurement oftemperature and relative humidity in theirbedroom for seven days, from January to April1987. This sample was stratified by estimatedbedroom relative humidity, to include all themost humid bedrooms and a one in four sampleof the remainder.'2 The present study wasbased on a subsample ofthis group. An attemptwas made to include all the children withwheeze, and all those whose parents had repor-ted visible mould in the home in the originalquestionnaire. A random sample ofone in eightof those with neither wheeze nor mould were

also asked to participate. Families who hadmoved house since the questionnaire surveywere excluded from the study.During the six months October 1987 to

March 1988 each home was visited four times(at approximately monthly intervals) for sam-pling of air in three rooms with a volumetricAndersen sampler.'5 In each home sampleswere taken in the living room and the child'sbedroom. If visible mould was a problemelsewhere in the house (21 homes), a thirdsample was taken in that room (other bedroomnine, bathroom 11, hallway one). Otherwise,the third sample was taken in the kitchen (67homes).

MYCOLOGICAL METHODSA six stage Andersen 1ACFM Viable ParticleSampler (Andersen 2000 Inc, Atlanta,Georgia, USA) was used to sample air forviable mould spores and yeasts. The intakeorifice was placed about 45 cm above floorlevel, and the instrument was operated accord-ing to the manufacturer's instructions exceptthat 9 0 cm disposable plastic Petri dishes wereused as collection plates. Each plate contained27 ml sterile malt agar (200 (w/v) malt extract,12", Agar No 3 (Oxoid)) with 20 units/mlbenzylpenicillin and 0-05 mg/ml streptomycinsulphate to inhibit bacterial growth. After 85litres of air had been sampled over threeminutes the plates were incubated at 250C forseven days. Counts of colony forming units(CFU) were computed from the numbers ofcolonies developing on the plates, correctionbeing made by the "positive hole" methodrecommended by the manufacturer.'5 Foridentification, fungi were isolated on to potatodextrose agar (Oxoid) plates incubated at 25°C,and identified by reference to standard texts'6and by comparison with reference strains.

Isolates of mycelial fungi (that is, the vege-tative, non-sporing hyphae), -which -becausethey did not sporulate in culture on eithermedium could not be identified, were platedout on 300 malt extract tannic acid agar to testfor production of diphenol oxidase.'6 Thosethat were positive were classified as basidio-mycetes capable of causing white rot of wood.Those that did not sporulate, did not producediphenol oxidase, and did not show the clampconnections characteristic of the classBasidiomycetes family were categorisedtogether as mycelia sterilia-that is, non-sporing fungi.

STATISTICAL ANALYSISStatistical analysis was performed by means ofthe Statistical Analysis System (SAS).'7 Inquantitative comparisons a logarithmic trans-formation was used for fungal counts to correctfor the positively skewed distribution. Forthis purpose, zero counts were treated as 0-1CFU/m3. Observations from the "no mouldand no wheeze" group were assigned a weightof 8 in the calculation of geometric means, toallow for the sampling fraction of 1/8 in thisgroup. Weighting was also used in comparisonsof means by one way analysis of variance, theGLM procedure in SAS'7 being used.

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Table 1 Relation between reported mould and wheeze in the population smrvey and the derivation of the study sampleNo of cifldren.with

Syvmptomn report Notv 1986: Wheie* past year No wheeze past year

Homp.e condition Nov 1986: Mould No mould Mould No mould Odds ratio (95% CL)Groutp: A B C D for wheeze v mould

Questionnaire survcy (9) 27 96 62 815 3 70 (2-22-615)Bedroom monitored (12) 15 30 38 247 3 25 (1 60-6 60)l arget sample 15 30 38 31Moved 2 5 6 5Refused 1 2 1 1No contact 1 0 2 0

Achieved sample 11 23 29 25

ResultsPOPULATION SURVEYThe original questionnaire survey obtainedusable data from 1000 (91",) of the 1095children selected as a random sample of thepopulation. Table 1 shows the numbers ofchildren who were reported by their parents tohave wheezed in the past year, and to havevisible mould growth in the home. The associa-tion between mould and wheeze was highlysignificant (p < 0 0001), and was largelyindependent of other social and housing vari-ables.4 Among the 330 children whose bedroomconditions were monitored for temperatureand relative humidity during January-April1987'2 the association was of similar strength(table 1).

SAMPLE SELECTION

Among the target sample for the present study,18 families were excluded because they hadmoved house, five refused to participate infurther studies, and no visits could be arrangedwith three families who initially agreed toparticipate. The overall response rate for sam-

pling of airborne fungi was therefore 77'U,, (88of the 114 homes in the target sample). Theresponse rate did not differ substantially in thefour "wheeze-mould" groups (table 1).Although the sample was chosen on the basis

of questionnaire data obtained one year earlier,29 (85") of the 34 children with wheezereported in the questionnaire were still wheez-ing during the winter of 1987-8. Our field-workers observed mould growth in few of thehomes that they visited. This probably reflectsthe exceptionally warm winter conditions dur-ing the period of the survey. The incidence ofmould growth was higher, however, in thehomes reported to be mouldy in 1986; five of 11

homes in group A (wheeze and mould); two of23 homes in group B (wheeze and no mould);five of 29 homes in group C (mould and no

wheeze); and one of 25 homes in group D (nomould and no wheeze).

DISTRIBUTION OF TOTAL MOULD COUNTSTable 2 shows the distribution of total (allspecies) counts of colony forming units ob-tained from each air sample, by sampling siteand wheeze-mould group. There was a widerange of values, but only three samples (twofrom group B, one from group C) had morethan 10 000 CFU/m3 of air. Six air samplescontained no viable moulds. In relation to thevariation between homes in each group, themedian counts for each group at each samplingsite were remarkably similar.

TYPES OF MOULD ISOLATEDNearly 50 species or genera of fungi were

identified in air samples. Table 3 shows theprincipal types isolated in each wheeze-mouldgroup. Yeasts were isolated on most occasions,but were not included in the total mould count.Spores ofPenicillium spp and Cladosporium sppwere isolated from at least one room in allhomes on every occasion. Together theyaccounted for about half of the total mouldcount. Only the heterogeneous group of air-borne mycelia sterilia appeared to bear anyrelation to the questionnaire reports of visiblemould in the home, being particularly evidentin the homes of children with wheeze andvisible mould growth (table 3). Less commonfungi included various Aspergillus species,most frequently A glaucus. A fumigatus, Anidulanus, and A terreus were occasionallyisolated, but never in large numbers.

MOULD COUNTS, WHEEZE, AND BRONCHIALLABILITYWeighted geometric mean mould counts forchildren with and without a history of wheezeand with and without exercise induced bron-chospasm are shown in table 4. The differences

Table 2 Distribution of total airborne mould counts (CFU per m3) by site ofsampling and subjectsgrouped accordingto the reporting of wheeze and mould, all visits combined

Room sampled: Living room Child's bedroom Other roomt

Wheeze: Yes Yes No No Yes Yes No No Yes Yes No NoMould: Yes No Yes No Yes No Yes No Yes No Yes NoGroup*: A B C D A B C D A B C D

Mininum 47 35 0 12 0 12 12 0 59 0 0 0Lower quartile 177 153 153 129 106 130 141 106 177 153 152 130Median 294 271 283 271 200 212 224 247 247 283 269 271Upper quartile 553 659 483 789 330 447 424 459 412 636 445 883Maximum 2895 38 594 4531 6038 3072 2695 41 265 7168 5049 36 946 3637 9534No of samples 41 91 112 95 41 91 111 95 41 91 111 96

*As in table 1.tSee text for details.

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Table 3 Principal types offungi identified in air samples, by wheeze-mould group

Number of homes in which thefungus was isolated

At any one visit At each visit

Wheeze reported: Yes Yes No No Yes Yes No NoMould reported: Yes No Yes No Yes No Yes NoGroup* A B C D A B C D

Yeastst 11 23 29 25 10 21 28 25Penicillium spp 11 23 29 25 11 23 29 25Cladosporium spp 11 23 29 25 11 23 29 25Sistotrema brinkmanii 11 23 28 24 5 10 12 11White rot basidiomycetes 11 23 28 25 5 7 14 5Mycelia sterilia 11 22 28 23 8 5 7 4Aspergillus versicolor 11 21 28 21 2 2 5 1Aureobasidium pullulans 11 18 22 15 0 1 0 2Botrytis cinerea 7 15 16 18 0 0 0 1No of homes visited 11 23 29 25 11 23 29 25

*As in table 1.tYeasts were excluded from the total mould counts.

between geometric mean counts for all speciescombined were small and inconsistent; countswere slightly lower in the homes of wheezychildren than in the homes of non-wheezychildren, but somewhat higher in the homes ofchildren with exercise induced bronchospasmthan in the remainder of the sample; thesedifferences, however, could easily haveoccurred by chance.The geometric mean counts for the five most

common groups of moulds in the homes ofchildren with and without wheeze and with andwithout exercise induced bronchoconstrictionare shown in table 4. For Penicillium spp,Cladosporium spp, Sistotrema brinkmanii, andwhite rot basidiomycetes the differences werenon-significant and in opposing directions forwheeze and bronchial lability. Non-sporingmycelia sterilia were generally found in lowconcentrations, but were present at higherlevels in the homes of both the wheezy childrenand those with exercise induced bronchocon-striction. When the homes of wheezy and non-wheezy children were compared, the differencein weighted geometric mean counts of myceliasterilia was significant (p < 0 01), but thissignificance test should be interpreted in thelight of the multiple comparisons that couldhave been made in table 4.

DiscussionThis study is the first to compare, in bothquantitative and qualitative terms, the indoormould flora of samples from homes of symp-tomatic and symptomless individuals from the

Table 4 Geometric mean* airborne mould counts (CFU per m3), all visits combined,by history of wheeze and degree of exercise induced bronchial lability during 1986-7

Wheeze in past year Bronchial lability > 1O%$

Room sampled Fungus Yes No (tt) Yes No (tt)

Living Total 304 311 -0-08 381 282 +1-52Child's Total 223 229 -0 07 285 206 + 128Other Total 309 314 -0-04 407 278 +1-67Pooled samples Total 276 281 -0 07 354 253 +1 63

Penicillium spp 39 55 -0 78 62 49 +0 75Cladosporium spp 16 12 +046 12 13 -0 30Sistotrema brinkmanii 5-1 3 4 +0 63 3-1 3-8 -0-18WPhite rot basidiomycetes 2-5 1-3 +1-45 1.0 1-7 -1-70Mycelia sterilia 2-1 0 7 +2-84 1 0 07 +1 11

No of children 34 54 26 62

*Log counts weighted for the different sampling fractions in groups A-D.tStudent's t test with 88 degrees of freedom.+Reduction in FEV, of > 10°,, of pre-exercise value, at either five or 10 minutes after six minutefree running exercise challenge.

general population. The viable mould countsthat we obtained from three minute air samplesmay not adequately reflect peaks and troughs ofexposure but, to put them in perspective, onlythree of the samples in our study approachedthe levels of 10 000-50 000 CFU/m3 that aretypical of a summer garden.'920 Occupationalexposures that are implicated in allergicalveolitis, such as the handling of mouldy hay,are associated with airborne spore burdensof a different order of magnitude, reaching1 600 000 000/m3 at times.2'Until recently there was little published

information on the extent to which indoormould growth affects the composition of thedomestic air spora in the United Kingdom.22 23A survey in 60 occupied council houses inLondon and three Scottish towns'8 found, aswe did, considerable differences in the totalairborne spore burden, not only betweenhomes but also with repeated sampling withinhomes. This variation is probably related todomestic activity, as spores are found in largenumbers in house dust (100 000-1 000 000/gdust.24 Homes with visible mould had some-what higher airborne mould counts, generallyin the range 1000-2000 CFU/m3, with skewingof the distribution towards high values.'8 Thissuggests that mould growth on walls doesincrease the average indoor spore burden(which is usually much higher than the outdoorburden in winter), though even these higherconcentrations are modest by comparison withsummer outdoor concentrations. The lowerspore counts in our study may reflect the mildwinter conditions that we encountered; but oursample of mouldy homes, being based onquestionnaire responses, probably includedfewer severe cases ofmould growth than homesthat have been the subject of complaint to localauthorities'8 or private landlords.Although valuable in comparing different

homes, volumetric sampling may under-estimate the true exposure of mobile people tofungal spores. Spores may be released fromhouse dust by movement in the room and enterconvection currents around the warm body,which are estimated to contribute 10% ofinspired air.25 The count of viable spores orcolony forming units of any one species, or ofall species combined, may be of limited clinicaland epidemiological relevance if spores fromdifferent species have different allergenicpotential,26 or if hypersensitivity reactions canalso be provoked by non-viable spores-whichpredominate, for example, in the air of someagricultural environments.27Many of the types of indoor mould fungi

isolated here and in the above studies,'82223however, were similar to those normally foundout of doors, so mould growth in most homesseems unlikely to influence the quality of theindoor fungal flora to an important extent.Furthermore, most of the species that wereidentified indoors in the present study, inclu-ding the highly allergenic spores ofBotrytis andAspergillus spp,26 were isolated on at least oneoccasion in most homes. This suggests thatmost people are exposed to some extent to awide range of fungi in the indoor air, quite

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apart from their shared exposure to airbornespores out of doors.Fewer asthmatic individuals have cutaneous

hypersensitivity to extracts ofmould fungi thanto house dust mite, but such reactions are notuncommon.2 Reported prevalence estimatesvary from 3 4o0 in Sweden to 80O in theUnited States.3 Among 656 asthmatic patientsattending an immunological outpatient clinicin London, 130o had positive skin test respon-ses to A fumigatus and 18o0" to other fungal

*4species.We found that the concentration of airborne

moulds in the home varies widely betweenhouses so that, if indoor moulds were ofaetiological relevance in childhood asthma, wewould expect airborne mould counts to behigher in the homes of wheezy children. Thefact that little difference was found is in strikingcontrast to the results of the original question-naire study. The discrepancy appears to arisepartly from bias in the reporting of symptoms9and partly because mild to moderate visibleindoor mould growth has only a minorinfluence on the airborne mould flora inside thehome, compared with dust raising householdactivities such as cleaning. We set out toinvestigate the possibility that reporting ofmould is more likely where a child has asthma.The absence of any difference between mediancounts of colony forming units in mouldyhomes with and without a wheezy child (groupsA and C) may not be remarkable as the airbornespore burden differed so little.between mouldyand non-mouldy homes.

Mycelia sterilia were cultured more fre-quently from air samples taken in the homesreported to be mouldy, and were present inhigher concentrations in the homes of wheezychildren. Further studies of these heterogen-eous fungi are required to confirm theseassociations. Particular attention is being paidto them in continuing studies ofboth viable andnon-viable airborne moulds.The appearance of mycelia in air samples is

consistent with several explanations. Firstly,the air samples may include spores from speciesthat do not sporulate in vitro on the culturemedia used, so that they cannot be assigned tospecies or genus. Alternatively, fragments ofmycelium from fungi that are not currentlysporing may become detached from their sub-strate and wafted into passing air currents.Thirdly, the substrate itself may become air-borne and carry non-sporing mould fungi withit. Faecal particles from the house -dust miteDermatophagoides pteronyssinus are known tobecome airborne and contain potent allergens,so the association between non-sporing fungalisolates and wheeze could perhaps reflect theoccurrence of moulds on mite faeces. Beforeany link can be confirmed between myceliasterilia and childhood asthma, the source,nature, and allergenicity of the various com-ponents should be clarified.The conclusions to be drawn from these

findings are limited by the methodologicaldifficulties of quantifying fungi in indoor airand by the relatively small number of homesstudied, but they are strengthened because the

relation of our study sample to the generalpopulation is well defined. Epidemiologicaldata such as these cannot exclude the possi-bility of clinically important idiosyncratic re-actions to domestic mould spores in a fewsusceptible individuals, nor do they address thepossible effects on health of exceptionally highmould spore concentrations in homes severelyaffected by mould.25On the other hand, they are relevant to

assessing the importance of damp, mouldyhousing as a public health problem and to thesetting of building standards.28 The confirma-tion of differential reporting of both symptomsand housing conditions in questionnaire datasuggests that further investigation of the linkbetween respiratory disease and damp, mouldyhousing should be based on valid and objectivemeasurements, preferably in samples that canbe related to the general population.

The original questionnaire survey was carried out while DPSheld a Wellcome research training fellowship, and 1986-7fieldwork was suppotied by the Asthma Research Council. The1987-8 fieldwork and subsequent mycological studies wereperformed at Heriot-Watt University under extramural contractfrom the Department of the Environment Building ResearchEstablishment. We wish to thank Ms P Ross for assistance withthe medical examinations, Ms B Somerville for visiting homesfor bedroom monitoring, and Dr A F Bravery and Mr C AHunter (at the Building Research Establishment) for theirvaluable advice throughout the fieldwork and for their com-ments on the text.

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4 Hendrick DJ, Davies RJ, d'Souza MF, Pepys J. An analysisof skin prick test reactions in 656 asthmatic patients.Thorax 1975;30:2-8.

5 Beaumont F, Kauffman HF, Sluiter HJ, de Vries K.Sequential sampling offungal air spores inside and outsidethe homes of mould-sensitive asthmatic patients: a searchfor a relationship to obstructive reactions. Ann Allergy1985;55:740-6.

6 Burr ML, Mullins J, Merrett TG, Stott NCH. Indoormoulds and asthma. JR Soc Health 1988;108:99-101.

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