p. 1 

Articles 

Indoor Dampness and Molds and Development of Adult-Onset Asthma : 

A Population-Based Incident Case-Control Study 

Maritta S. Jaakkola,' Henrik Nordman,I Ritva Piipari,I Jukka Uitti,2 Jukka Laitinen,3 Antti Karjalainen,I Paula 

Hahtola,4 and Jouni J. K. Jaakkola5"s 

Finnish Institute of Occupational Health, 'Helsinki and zTampere, Finland; Departments of 3CIinical Physiology and 'Pulmonary 

Medicine, Tampere University Hospital, Tampere, Finland; 5Environmental Epidemiology Unit, Department of Public Health, University 

of Helsinki, Helsinki, Finland; 6Environmental Health Program, Nordic School of Public Health, G6teborg, Sweden 

Previous cross-sectional and prevalent case-control studies have suggested increased risk of 

asthma in adults related to dampness problems and molds in homes. We conducted a populationbased incident case-control study to assess the effects of indoor dampness problems and molds at 

work and at home on development of asthma in adults . We recruited systematically all new cases 

of asthma during a 2.5-year study period (1997-2000) and randomly selected controls from a 

source population consisting of adults 21-63 years old living in the Pirkanmaa Hospital district, 

South Finland. The dinically diagnosed case series consisted of 521 adults with newly diagnosed 

asthma and the control series of 932 controls, after we excluded 76 (7 .5%) controls with a history 

of asthma. In logistic regression analysis adjusting for confounders, the risk of asthma was related 

to the presence of visible mold and/or mold odor in the workplace (odds ratio, 1 .54; 95% confidence interval, 1 .01-2.32) but not to water damage or damp stains alone. We estimated the fraction of asthma attributable to workplace mold exposure to be 35 .1% (95% confidence interval, 

1 .0-56.9%) among the exposed. Present results provide new evidence of the relation between 

workplace exposure to indoor molds and adult-onset asthma. Key words asthma, case-control study, 

molds, occupational exposure, population-based . Environ Health Perspect 110:543-547 (2002) . 

[Online 4 April 2002] 

http://ehpnetl .niehs.nih.gov/docs/2002/110p543-547jaakkolalabstract.html 

Indoor dampness and mold problems are universal and thus are potentially of major public 

health importance (1-11) . Such problems 

have been surprisingly common in countries 

with cold climates, such as Finland, Sweden, 

and Norway (4,5,9, 11) . The major reasons 

for the high frequency of such problems in 

cold climates may be insufficient maintenance 

of the buildings and construction of tight 

buildings to conserve energy accompanied by 

inadequate ventilation. Residential dampness 

problems have been related to increased risk 

of asthma and asthma-related symptoms in 

children (1,2,4,6,8,12-15) and in adults 

(7,9,13,15-20) . However, we did not identify 

any epidemiologic study of workplace indoor 

dampness and mold problems and asthma, 

and only four studies have evaluated potential 

effects of such problems on wheezing 

(5,10,21,22) . These studies were carried out 

in either daycare centers or offices. Most of 

the studies among adults were cross-sectional 

or prevalent case-control studies in design, 

and almost all of them based the diagnosis of 

asthma or asthma-related symptoms on selfreport in questionnaires or interviews . 

The objective of our study was to assess 

the role of dampness problems and molds at 

work and at home in the development of 

asthma in working-age population . We 

recruited incident cases of asthma, the diagnosis being verified with clinical examinations. We also evaluated some personal 

characteristics, such as age, sex, and smoking, 

as potential indicators of sensitivity to the 

adverse effects of dampness problems . 

Methods 

Study Design 

This study was a population-based incident 

case-control study. The source population 

consisted of adults 21-63 years old living in 

the Pirkanmaa Hospital district . This district 

is a geographically defined administrative 

area in South Finland with a population of 

440,913 inhabitants in 1997. Our goal was 

to recruit all the new cases of asthma in the 

source population during the study. We 

selected controls randomly from the source 

population based on 1997 census data . The 

ethics committees of the Finnish Institute of 

Occupational Health and the Tampere 

University Hospital approved the study. 

Definition and Selection of Cases 

We systematically recruited all the new cases 

of asthma, first in the city of Tampere 

beginning on 15 September 1997, and then 

in the whole Pirkanmaa Hospital district 

from 10 March 1998 to 31 March 2000. 

We recruited patients at all health care facilities diagnosing asthma, including the 

Department of Pulmonary Medicine at the 

Tampere University Hospital, offices of the 

private-practicing pulmonary physicians in 

the region, and public health care centers. 

As an additional route of case selection, the 

National Social Insurance Institution of 

Finland invited all patients to participate 

whose reimbursement rights for asthma 

medication began during the period 1 

September 1997 through 1 May 1999 and 

who had not yet participated . 

We applied the following diagnostic criteria for asthma: a) history of at least one 

asthmalike symptom (prolonged cough, 

wheezing, attacks of or exercise-induced dyspnea, or nocturnal cough or wheezing) and 

b) demonstration of reversibility in airway 

obstruction in lung function investigations . 

Table 1 presents lung function findings 

accepted to demonstrate reversibility . These 

diagnostic procedures correspond to the recommendations of the National Asthma 

Program in Finland (23) . 

We selected as cases all the confirmed 

cases of asthma fulfilling the general eligibility criteria . A total of 362 cases (response 

rate, 90%) participated through the health 

care system, and 159 cases participated 

through the National Social Insurance 

Institution (response rate, 78%), totaling 521 

cases overall. 

Selection of Controls 

We randomly selected the controls from the 

source population using the national population registry, which has full coverage of the 

population . We applied the general eligibility criteria for controls . After up to three 

invitation letters and phone calls, 1,016 participated in the study (response rate, 67% of 

total invited population, or 80% of those 

who had a phone number in the Pirkanmaa 

area) . Previous or current asthma was 

reported by 76 (7 .5%); six persons were 

Address correspondence to M.S . Jaakkola, Finnish 

Institute of Occupational Health, Topeliuksenkatu 

41 aA, FIN-00250 Helsinki, Finland. Telephone: 

358-9-4747-2249 . Fax: 358-9-4747-2009 . E-mail: 

Maritta.Jaakkola@occuphealth .fi 

We thank our research nurses L. Yrjanheikki, M. 

Soukkanen, and M. Aalto and all the health care 

workers who participated in recruiting study subjects at the Tampere University Hospital, health 

care centers, private practices, and the National 

Social Insurance Institution of Finland. 

This study was supported by grants from the 

Ministry of Social Affairs and Health of Finland 

and the Finnish Work Environment Fund . 

Received 24 October 2001 ; accepted 10 

December 2001 . 

Environmental Health Perspectives " VOLUME 110 1 NUMBER 5 1 May 2002 543 
p. 2 

Articles " Jaakkola et al . 

older than 63 years, and two returned 

incomplete questionnaires . After excluding 

these persons, our study population included 

932 controls . 

Exposure Assessment 

We based exposure assessment on questionnaire information about water damage, 

damp stains and other marks of structural 

dampness, visible mold, and mold odor, 

both at home and indoors at work (4,5) . For 

water damage, damp stains, and visible 

mold, we asked for information about their 

occurrence during the past year, 1-3 years 

before, or > 3 years before . For mold odor, 

we asked the subject about occurrence during the past year and to indicate if such odor 

appeared almost daily, 1-3 days a week, 1-3 

days a month, < I day a month, or never. 

Data Collection 

At the Tampere University Hospital, we 

recruited cases at their first visit for suspected 

asthma, and we verified the diagnosis in clinical examinations . At the other health care 

facilities, cases were recruited immediately 

when their asthma diagnosis was verified . 

We applied the same protocol for diagnosing 

asthma at all health care facilities . The 

National Social Insurance Institution invited 

the cases 6 months to 2 years after their diagnosis was established . For these patients, we 

confirmed the date and criteria of the asthma 

diagnosis from their medical records to 

ensure that the diagnosis of asthmatics 

included in our study fulfilled our criteria . 

For all cases, we verified from their medical 

records that they did not have a previous 

asthma diagnosis . Eligible subjects were 

invited to participate in the study, and 

informed consent was asked by their physician or through a letter sent by the National 

Social Insurance Institution . The cases 

answered the questionnaire at the time of 

recruitment . Recruitment of controls took 

place at regular intervals throughout the study 

period . Informed consent was requested in 

the letter and returned in a prepaid envelope 

to the research nurse of the study project . 

Measurement Methods 

Questionnaire. The self-administered questionnaire, modified from the Helsinki Office 

Environment Study questionnaire (24,25) to 

be used in a general population, included six 

sections: 1) personal characteristics, 2) health 

information, 3) active smoking and environmental tobacco smoke exposure, 4) occupation and work environment, 5) home 

environment, and 6) dietary questions . 

Lung function measurements . We 

applied the same lung function protocol to 

all patients with suspected asthma . The only 

exception was patients recruited through the 

National Social Insurance Institute, for 

whom we obtained lung function data by 

abstracting from the medical records . 

Baseline spirometry . For all patients with 

suspected bronchial asthma, we recorded vital 

capacity and flow-volume curves with a pneumotachygraph spirometer connected to a 

computer and using a disposable flow transducer (Medikro 905; Medikro Ltd., Kuopio, 

Finland) . We carried out the measurements 

according to the standards of the American 

Thoracic Society (26) . We judged presence of 

obstruction using the reference values derived 

from a Finnish population (27) . 

Bronchodilation test . After baseline 

spirometry, all patients received 400 pg of 

salbutamol (albuterol) with a spacer and 

performed spirometric flow-volume curves 

after 10 min. 

Peak expiratory flow (PEF) follow-up . 

All patients performed PEF follow-up for at 

least 2 weeks with a mini Wright meter . We 

instructed subjects to carry out measurements twice a day, in the morning and in 

Table 1 . Lung function findings confirming reversibility of obstruction among asthma cases, Finnish 

Environment and Asthma Study 1997-2000. 

Lung function criteria 

1 . Significant improvement in response to short-acting bronchodilating medication in a bronchodilator test . Criteria 

for significant changes: 

FEV, a 15% 

FVC Z 15% 

PEF Z 23% 

and/or 

2. Daily variationa z 20% and/or z 15% improvement' in response to short-acting bronchodilating medication during 

at least 2 days in a 2-week diurnal PEF follow-up . 

and/or 

3. Significant improvement in spirometric lung function (criteria given in item 1) and/or a 20% improvement in the 

average PEF level in response to a 2-week oral steroid treatment. 

Abbreviations: FEVi, forced expiratory volume in 1 sec; FVC, forced vital capacity; PEF, peak expiratory flow. 

'Calculated according to the standard practice of the Tampere University Hospital : maximum daily variation = (highest 

PEF value during the day- lowest PEF value during the day)/highest PEF value during the day ; bronchodilator response = 

(highest PEF value after bronchodilating medication - highest PEF value before medication)/highest PEF value before 

medication . Table 2 . Characteristics of the study population, Finnish Environment and Asthma Study 1997-2000. 

Cases Controls 

Characteristic No. Percent No. Percent 

Total 521 932 

Sex 

Male 175 33 .6 438 47 .0 

Female 346 66 .4 494 53 .0 

Age (years) 

21-29 108 20 .7 141 15.1 

30-39 107 20 .5 224 24.0 

40-49 125 24 .0 254 27 .3 

50-59 140 26 .9 240 25.8 

60-63 41 7.9 73 7.8 

Parental allergic diseases 

Maternal allergy 85 16 .3 108 11 .6 

Paternal allergy 47 9 .0 48 5.2 

Maternal asthma 66 12 .7 64 6 9 

Paternal asthma 62 11 .9 48 52 

Any 186 35.7 204 21 .9 

Education' 

No vocational schooling 107 20.6 154 16 .6 

Vocational course 89 17 .2 104 11 .2 

Vocational institution 149 28 .7 271 29 .2 

College-level education 113 21 .8 261 28 .1 

University or corresponding 61 11 .8 138 14 .9 

Smokingb 

Never 239 46 .1 487 52 .4 

Formerly 133 25 .7 203 21 .8 

Currently 146 28 .2 240 258 

Environmental tobacco smoke 

In the workplace 89 17 .1 130 13 .9 

In the home 30 5 .9 52 5.6 

Pets at home 

Sometimes 387 74.3 663 71 .1 

Any work exposure' 313 60 .1 579 62 .1 

'Information on education was missing for six subjects . °Information on smoking was missing for five subjects . `Selfreported exposure to sensitizers, dusts, and/or fumes, except for exposure to molds . 544 VOLUME 110 1 NUMBER 51 May 2002 " Environmental Health Perspectives 
p. 3 

Articles " Indoor molds and adult-onset asthma 

the evening. During the second week, subjects performed measurements before and 15 

min after short-acting bronchodilating medication . Subjects recorded all three readings, 

and we used the highest value in the analyses . 

Steroid treatment response. We recommended that physicians give a 2-week oral 

steroid treatment to those with a strong suspicion of asthma, if the other diagnostic tests 

were negative . The patient was asked to perform 2 weeks of PEF follow-up during this 

treatment, and spirometry was carried out 

again at the end of this treatment period to 

judge the response. 

Statistical Methods 

We used exposure odds ratio (OR) to quantify the relations between exposures and 

outcome, and estimated adjusted OR in logistic regression analysis . We used the following 

covariates to adjust for potential confounding: 

sex, age, parental atopy or asthma, education 

(as an indicator of socioeconomic status), personal smoking, dampness and mold problems 

in the home or at work, exposure to environmental tobacco smoke, any history of pets in 

the home, and self-reported occupational 

exposure to sensitizers, dusts or fumes (except 

self-reported exposure to molds) . 

We studied the independent predictive 

value of the four exposure indicators (water 

damage, damp stains, visible mold, and 

mold odor) in the workplace (for those 

working at least 50% of their workday 

indoors) and in the home by including all 

the exposure indicators as well as covariates 

Table 3. Distribution of exposure indicators in cases and controls, Finnish Environment and Asthma Study 

1997-2000. Exposure indicator No. 

Cases Controls 

Work 

Water damagea 

No 458 

Yes, during past 12 months 32 

Yes, 1-3 years ago 20 

Yes, > 3 years ago 11 

Damp stains or paint peelinga 

No 431 

Yes, during past 12 months 66 

Yes, 1-3 years ago 18 

Yes, > 3 years ago 6 

Visible molda 

No 487 

Yes, during past 12 months 24 

Yes, 1-3 years ago 6 

Yes, > 3 years ago 4 

Mold odor during past 12 months' 

No 462 

Yes, almost daily 25 

Yes, 1-3 days per week 11 

Yes, 1-3 days per month 7 

Yes, < 1 day per month 16 

Home 

Water damageb 

No 462 

Yes, during past 12 months 11 

Yes, 1-3 years ago 10 

Yes, > 3 years ago 33 

Damp stains or paint peelingb 

No 418 

Yes, during past 12 months 54 

Yes, 1-3 years ago 22 

Yes, > 3 years ago 27 

Visible moldb 

No 494 

Yes, during past 12 months 18 

Yes, 1-3 years ago 5 

Yes, > 3 years ago 3 

Mold odor during past 12 months 

No 467 

Yes, almost daily 17 

Yes, 1-3 days per week 7 

Yes, 1-3 days per month 10 

Yes, < 1 day per month 20 

Percent No. Percent 

87 .9 811 87 .0 

6.2 53 5 .7 

3.8 42 4 .5 

2 .1 26 2 .8 

82 .6 761 81 .7 

12 .7 108 11 .6 

3.5 32 3.4 

1 .2 31 3.3 

93,4 890 95 .5 

4 6 30 3.2 

12 10 11 

0.8 2 0 2 

88 .7 846 90 .7 

4 .8 39 4 .2 

2.1 13 1 .4 

1 .3 9 1 .0 

3.1 25 2 .7 

887 817 87 .7 

2 .1 15 1 .6 

1 .9 27 2.9 

6 .3 61 6.5 

80 .2 744 79 .8 

10 .4 85 9.1 

4.2 51 5.5 

5.2 49 5.3 

947 875 93 .9 

3.5 28 3.0 

1 .0 18 1,9 

0.6 10 1 .1 

89 .6 846 90 .7 

3.3 23 2.5 

1 .3 8 0 .9 

1 .9 20 2 .1 

3.9 35 3 .6 

'Yes categories included only those who worked indoors at least 50% of their work day ; others are included in the no 

category . "Do not know" was answered by 5 cases and 12 controls for water damage, three controls for damp stains, 

and one case and one control for visible mold . 

in the model. We also elaborated the role of 

exposure time period by fitting time-specific 

exposure variables. We combined occurrence 

of dampness and mold problems during different time periods because we detected no 

meaningful trends according to the time 

specificity of exposure (data not shown) . We 

combined any visible mold and/or mold 

odor in the workplace to represent the main 

exposure parameter. These two exposure 

indicators were closely related and had 

strong overlap, so including them separately 

in the models was not meaningful. The reference category consisted of those reporting 

no mold or dampness exposure . We also 

analyzed the data after excluding patients 

recruited by the National Social Insurance 

Institution. 

We systematically studied potential 

modification of the relation between main 

exposure parameter and risk of asthma by 

comparing the adjusted ORs by sex, age 

(20-29, 30-49, and 50-63 years), parental 

atopy or asthma (yes/no), and smoking 

(never, former, current) . 

Finally, we quantified the impact of 

exposure as an attributable fraction (28) or 

etiologic fraction (29), providing the fraction 

of exposed cases for whom the disease is 

attributable to the exposure (28) . We calculated the attributable fraction (AF) 

AF = (OR- 1)/OR, 

where OR is the adjusted OR due to the 

exposure of interest, an unbiased estimate of 

incidence ratio in a population-based 

case-control study (29) . We calculated the 

95% confidence interval (CI) using the corresponding interval of OR. 

Results 

Characteristics and Exposure of 

Cases and Controls 

A larger proportion of cases than controls 

were women, young, current smokers, and 

exposed to environmental tobacco smoke 

and to pets ; had lower education ; and 

reported a history of parental allergic diseases 

(Table 2) . 

A larger percentage of cases than controls 

reported presence of visible mold (6 .6% vs . 

4.5%) and mold odor (11 .3% vs . 9.3%) in 

the workplace (Table 3) . The frequency distributions of water damage and damp stains 

or paint peeling in the workplace and of all 

the four exposure indicators in the home 

were similar among cases and controls . 

Indoor Dampness Problems and 

Molds and the Risk of Asthma 

The risk of asthma was related to the presence of visible mold and/or mold odor in the 

Environmental Health Perspectives " VOLUME 110 1 NUMBER 51 May 2002 545 
p. 4 

Articles " Jaakkola et al . 

workplace, but not to water damage or 

damp stains alone, as shown in Table 4. The 

adjusted OR for any exposure to visible 

mold or mold odor was 1 .54 (95% CI, 

1 .01-2 .32) . The risk of asthma was related 

to none of the exposure indicators in the 

home. The results were essentially similar in 

the analyses that excluded cases recruited 

through the National Social Insurance 

Institution . We estimated the fraction of 

asthma attributable to workplace mold exposure to be 35 .1% (95% CI, 1 .0-56.9%) 

among the exposed . 

The relation between workplace mold 

exposure and the risk of asthma was slightly 

stronger in women than in men (Table 5) . 

The relation was strongest in the youngest 

age group and stronger in current smokers 

than in former smokers or never smokers. 

The relative risk was essentially similar in 

those with and without parental atopy. 

Discussion 

We found a significantly increased risk of 

new asthma in adults in relation to the presence of visible mold and/or mold odor in the 

workplace, whereas water damage or damp 

stains alone were not associated with asthma. 

The mechanisms by which indoor dampness 

problems could lead to an increased risk of 

asthma are not well understood, and several 

potential causes have been suggested : molds, 

bacteria, house dust mites, and enhanced 

emission of chemicals from surface materials 

(9,15) . Our results emphasize the role of 

molds (and possibly bacteria) as an important cause of asthma, rather than dampness 

per se . Potential mechanisms by which 

indoor molds could induce asthma include 

immunoglobulin E-mediated hypersensitivity reactions, toxic reactions caused by mycotoxins, and nonspecific inflammatory 

reactions caused by irritative volatile organic 

compounds produced by microbes or cell 

wall components, such as 1,3-(3-D-glucan 

and ergosterol (9,30-32) . Different species 

of molds may induce asthma by different 

mechanisms, or molds may induce health 

effects by combined mechanisms (32) . 

The risk of asthma was not associated 

with the presence of dampness or molds at 

home in this study . We have no reason to 

believe that effects of similar exposures at 

home and at work would be different . 

Rather, the difference in effect estimates in 

our study are likely explained by more extensive mold problems at work than at home. 

We did not quantify the extent of such 

problems, but it is likely that in the workplace people do not notice small dampness 

problems easily, because they change work 

areas often, and thus more extensive mold 

growth may develop . In addition, influencing the work environment is often more difficult . At home, people tend to pay attention 

to water damage and repair it before more 

advanced mold problems develop, because 

such damage reduces the value of the property. In 1998 in the Pirkanmaa area, 67% of 

the population owned the residences in 

which they lived . Other potential explanations for these differences include, for example, ventilation systems of workplaces 

favoring the spread of molds and their 

metabolites into indoor air . The attributable 

fraction of asthma due to workplace mold 

was surprisingly high: 35% among the 

exposed cases . 

We found that women, the young, and 

smokers are especially susceptible to the 

effects of workplace molds. The mechanisms 

of such susceptibility are not known and 

should be studied further . The young and 

women may have more extensive exposures, 

because they are often in lower positions in 

the workplace and therefore have less influence on their work environment . Also, 

modification of immunologic or other 

inflammatory reactions may play a role in 

sensitivity, at least in current smokers . 

Finnish population, and its medication files 

have practically a full coverage of asthmatics 

who fulfill the diagnostic criteria required for 

reimbursement in Finland. The response 

rate among the control population was also 

relatively high, especially among those who 

had a phone number in the Pirkanmaa 

region and were likely to really live in this 

area during our study period . Thus, any 

major selection bias is unlikely in our study . 

To reduce information bias, we introduced the study to the participants as a study 

on environmental factors and asthma in general (the Finnish Environment and Asthma 

Study), with no special focus on mold and 

dampness problems. We collected information on exposures in a similar way from cases 

and controls . The physicians responsible for 

the diagnostic procedures of asthma were 

unaware of the questionnaire responses of 

the study subjects . Our finding of an 

increased risk of asthma in relation to workplace exposure but not in relation to home 

exposure supports unbiased reporting ; it is 

unlikely that subjects would associate their 

symptoms to a specific exposure in one environment but not in the other. In the analyses excluding cases recruited by the National 

Social Insurance Institution (i .e ., some time 

after their diagnosis was made), the OR 

related to workplace mold exposure 

remained increased (1 .38) but was slightly 

reduced . This indicates that some overreporting of workplace exposure may have 

taken place, but this does not explain the 

effect entirely. On the other hand, studies 

comparing self-reported dampness with site 

visits have usually shown that subjects tend 

to underestimate their exposures (7,9, 11) . 

Thus, self-report of exposures may have led 

to some underestimation of the risks in our 

study (e .g ., the risks for home exposures) . 

Validity Issues 

We were able to recruit a high proportion of 

new cases of asthma by a thorough recruitment through the health care system 

(response rate, 90%) and with the help of 

the National Social Insurance Institution 

providing us a route to reach those asthmatics that we missed by our recruitment system (response rate, 78%) . The health 

insurance provided by the National Social 

Insurance Institution covers the whole 

Table 4. Adjusted ORs of asthma in relation to exposure to mold and dampness in the workplace and at 

home, Finnish Environment and Asthma Study 1997-2000. 

Exposure/history 

Work 

Visible mold or mold odor 

Damp stains or paint peeling 

Water damage 

Home 

Visible mold or mold odor 

Damp stains or paint peeling 

Water damage 

OR' 95% CI 

1 .54 1 .01-2.32 

0.84 0.56-1.25 

0.91 0.60-1.39 

0.98 0.68-1 .40 

1 .02 0.73-1 .41 

0 .90 0.61-1 .34 

'Adjusted for sex, age, parental atopy/asthma, education, smoking, environmental tobacco smoke exposure, pets, work 

indoors, self-reported occupational exposures, and other exposure indicators shown in the table . 

Table 5. Adjusted ORs of asthma in relation to visible mold and/or mold odor in the workplace 

according to potential effect modifiers, Finnish 

Environment and Asthma Study 1997-2000. 

Study population OR' 95% CI 

All 1 .54 1 .01-2.32 

Sex 

Male 1 .26 062-2.54 

Female 1 .67 1 .00-2.79 

Age (years) 

20-29 2.98 0.96-9.27 

30-49 1 .31 0 .75--2 .30 

50-63 1 .46 0 .65-3.29 

Parental atopy 

Yes 1 .57 0.57-4.31 

No 1 .61 1 .02-2.55 

Smoking 

Currently 3.05 1 .14-8.14 

Formerly 0.83 0.32-2.10 

Never 1 .63 0.92-2.90 

'Adjusted for sex, age, parental atopy/asthma, education, smoking, environmental tobacco smoke exposure, 

pets, work indoors, self-reported occupational exposures, and other exposure indicators. 

546 VOLUME 110 1 NUMBER 51 May 2002 " Environmental Health Perspectives 
p. 5 

Articles " Indoor molds and adult-onset asthma 

We defined asthma on the basis of objective 

clinical findings to eliminate information 

bias concerning the outcome. 

We were able to adjust for a number of 

potential confounders (see "Statistical 

Methods") in logistic regression analysis to 

eliminate these factors as potential explanations for our results . We adjusted for parental 

atopy to control for genetic predisposition, 

but not for subjects' own atopy, because this 

may be in the causal pathway for effects of 

indoor molds. 

Synthesis with Previous Knowledge 

Earlier studies on indoor dampness and 

mold problems in adults have been mainly 

cross-sectional or prevalent case-control 

studies in design ; therefore, our results cannot be compared directly with them . One 

population-based study from Sweden 

assessed adult-onset asthma based on questionnaire reports of asthma (20) . A significant OR of 2 .2 was reported in relation to 

visible mold at home, whereas visible dampness alone was not significantly related to 

asthma . The Swedish study assessed the 

onset of asthma retrospectively based on selfreported information about the year of diagnosis . The subjects had to recall both the 

year of diagnosis and exposures as far back as 

14 years before, which makes the study vulnerable to recall bias . The Swedish study did 

not adjust for or estimate the risk related to 

workplace mold problems. 

We identified no earlier study that had 

assessed the relation between workplace 

dampness and mold problems and the risk of 

asthma . A previous study in Finnish daycare 

nurses reported the risk of wheezing related 

to workplace exposure, while adjusting for 

home exposure (S) . The OR was 1 .66 when 

water damage was present and 1 .28 when 

water damage and mold odor both were present. These estimates are close to our OR of 

asthma among women (1 .67) . In addition, 

three other studies reported risk estimates of 

wheezing in relation to workplace dampness 

or mold exposures. A study from the United 

States reported an OR of 2 .8 for usual 

wheezing and 1 .9 for occasional wheezing in 

association with mold exposure in problem 

office buildings in Florida (22) . A study of 

Taiwanese daycare centers found an 

increased risk of wheezing in relation to 

stuffy odor (OR, 1 .38), visible mold (OR, 

1 .39), and water damage (OR, 1.32) (21) . 

Another Taiwanese study of office workers 

found similar ORs for chest tightness and 

chest pain (10) . 

Two Dutch studies assessed the risk of 

asthma related to residential dampness stratified by sex. In one of them (18) the risk was 

similar in men (OR, 1 .29) and women (OR, 

1 .25), whereas the other (13) found, in 

agreement with our study, a greater risk in 

women (OR, 4.16) than in men (OR, 1 .15) . 

The Swedish study (20) found an essentially 

similar risk of asthma related to visible mold 

growth among men (2 .7) and women (2 .0). 

Modification by age, genetic predisposition, 

or smoking status has not been previously 

studied. 

Conclusion 

The present results provide new evidence of 

the relation between workplace exposure to 

indoor molds and development of asthma in 

adulthood . Our findings suggest that indoor 

mold problems constitute an important 

occupational health hazard . 

REFERENCES AND NOTES 

1 . Platt SD, Martin CJ, Hunt SM, Lweis CW. Damp housing, 

mould growth, and symptomatic health state . Br Mad J 

298:1673-1678(19891. 

2. Dales RE, Zwanenburg H, Burnett R, Franklin CA . 

Respiratory health effects of home dampness and molds 

among Canadian children . Am J Epidemiol 134 :196-203 

(1991) . 

3. Brunekreef B . Associations between questionnaire 

reports of home dampness and childhood respiratory 

symptoms . Scl Total Envuon 127:79-89 (1992) . 

4. Jaakkola JJK, Jaakkola N, Ruotsalainen R. Home dampness and molds as determinants of respiratory symptoms 

and asthma in pre-school children. J Exp Anal Environ 

Epidermal 3 :129-142 (1993) . 

5. Ruotsalamen R, Jaakkola N, Jaakkola JJK. Dampness 

and molds in day-care centers as an occupational health 

problem . Int Arch Occup Environ Health 66 :369-374 

(1995) . 

6. Maier WC, Arrighi HM, Morray B, Llewellyn C, Redding 

GJ . Indoor risk factors for asthma and wheezing among 

Seattle school children . Environ Health Perspect 

105 :208-214 (1997) . 

7. Williamson IJ, Martin CJ, McGill G, Monie RDH, Fennerty 

AG . Damp housing and asthma : a case-control study . 

Thorax 52 :229-234 (1997) . 

8. Nafstad P, Die L, Mehl R, Gaarder PI, Ledrup-Carlsen KC, 

Batten G, Magnus P, Jaakkola JJK . Residential dampness problems and symptoms and signs of bronchial 

obstruction in young Norwegian children . Am J Respir 

Crit Care Mad 157 :410-414 (1998). 

9 . Norback D, Bjornsson E, Janson C, Palmgren U, Boman 

G . Current asthma and biochemical signs of inflammation in relation to building dampness in dwellings. Int J 

Tuberc Lung Dis 3 :368-376 (1999) . 

10. Wan G-H, Li C-S . Dampness and airway inflammation 

and systemic symptoms in office building workers . Arch 

Environ Health 54 :58-63 (1999) . 

11 . Nevalainen A, Partanen P, Jaaskelainen E, Hyvarinen A, 

Koskinen 0, Meklin T, Vahteristo M, Koivisto J, Husman 

T . Prevalence of moisture problems in Finnish houses. 

Indoor Air Suppl 4 :4549 (1998) . 

12 . Brunekreef B, Dockery DW, Speizer FE, Ware JH, 

Spengler JD, Ferris BG . Home dampness and respiratory 

morbidity in children . Am Rev Respir Dis 140:1363-1367 

(1989) . 

13 . Waegemaekers M, Van Wageningen N, Brunekreef B, 

Boleij JSM . Respiratory symptoms in damp houses . A 

pilot study . Allergy 44 :192-198 (1989) . 

14. Spengler JD, Neas L, Dockery DW, Speizer F, Ware J, 

Raizanne M . Respiratory symptoms and housing characteristics. Indoor Air 4:72-82(1994). 

15. Bornehag C-G, Blomquist G, Gyntelberg F, Jarvholm B, 

Malmberg P, Nordvall L, Nielsen A, Pershagen G, Sundell 

J . Dampness in buildings and health . Nordic interdisciplinary review of the scientific evidence on associations 

between exposure to dampness in buildings and health 

effects (NORDDAMP) . Indoor Air 11 :72-86 (2001) . 

16. Hyndman SJ . Housing dampness and health amongst 

British Bengalis in East London . Soc Sci Mad 30 :131-141 

(1990) . 

17 . Dales RE, Burnett R, Zwanenburg H . Adverse health 

effects among adults exposed to home dampness and 

molds. Am Rev Respir Dis 143 :505-509 (1991). 

18 . Brunekreef B . Damp housing and adult respiratory symptoms . Allergy 47:498-502 (1992) . 

19 . Hu FB, Persky V, Flay BR, Richardson J . An epidemiological study of asthma prevalence and related factors 

among young adults . J Asthma 34 :67-76 (1997). 

20 . Thorn J, Brisman J, Toren K . Adult-onset asthma is associated with self-reported mold or environmental tobacco 

smoke exposures in the home. Allergy 56 :287-292 (2001) . 

21 . Li C-S, Hsu C-W, Lu C-H . Dampness and respiratory 

symptoms among workers in daycare centers in a subtropical climate . Arch Environ Health 52 :68-71 (1997) . 

22 . Hodgson MJ, Morey P, Leung W-Y, Morrow L, Miller D, 

Jarvis BB, Robbins H, Halsey JF, Storey E . Building-associated pulmonary disease from exposure to Starchybotrus 

chartatum and Aspergillus versicolor. J Occup Environ 

Mad 40:241-249 (1998). 

23 . Committee on National Asthma Program in Finland . 

Asthma Program 1994-2004 [in Finnish]. Report No. 16. 

Helsinki:Ministry of Social Affairs and Health Publications, 

1994. 

24. Jaakkola JJK, Miettinen P . Type of ventilation system in 

office buildings and sick building syndrome . Am J 

Epidemiol 141 :755-765 (1995) . 

25. Jaakkola MS, Jaakkola JJK . Office equipment and supplies : a modern occupational health concern? Am J 

Epidemiol 150:1223-1228 (1999). 

26. American Thoracic Society . Standardization of spirometry, 

1994 update . Am J Respir Crit Care Mad 152:1107-1136 

(1995). 

27. Viljanen AA, Halttunen PK, Kreus K-E, Viljanen BC . 

Spirometric studies in nonsmoking, healthy adults . 

Scand J Clin Lab Invest 42(suppl 159) :5-20 (1982) . 

28. Greenland S. Applications of stratified analysis methods . 

In : Modern epidemiology (Rothman KJ, Greenland S, 

ads) . 2nd ad. Philadelphia :Lippincott-Raven, 1998;29Cr297 . 

29. Miettinen OS . Proportion of disease caused or prevented 

by a given exposure, trait or intervention . Am J Epidemiol 

99 :325-332 (1974) . 

30. Husman T . Health effects of indoor-air microorganisms . 

Scand J Work Environ Health 225-13 (19961 . 

31 . Thorn J, Rylander R. Airways inflammation and glucan in a 

rowhouse area . Am J Respir Crit Care Mad 157 :1798-1803 

(1998) . 

32. Johanning E, Landsbergis P, Gareis M, Yang CS, Olmsted 

E . Clinical experience and results of a sentinel health 

investigation related to indoor fungal exposure . Environ 

Health Perspect 107(suppl3) :489-494119991 . 

Environmental Health Perspectives " VOLUME 110 1 NUMBER 51 May 2002 547