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

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

Population-Based Incident Case-Control Study

Maritta S. Jaakkola,1 Henrik Nordman,1 Ritva Piipari,1 Jukka Uitti,2

Jukka Laitinen,3 Antti Karjalainen,1 a Hahtola,4 and Jouni J.K.

Jaakkola5,6

Finnish Institute of Occupational Health, 1Helsinki and 2Tampere,

Finland; Departments of 3Clinical Physiology and 4Pulmonary

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, Göteborg, Sweden

Abstract

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 population-based

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 clinically

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://ehpnet1.niehs.nih.gov/docs/2002/110p543-547jaakkola/

abstract.html

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@...

We thank our research nurses L. Yrjänheikki, 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.

Introduction

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 self-report 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 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 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, < 1 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 µg 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 meter. We

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

morning and in 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 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 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-

ß-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.

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 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). 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

self-reported 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 (5). 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.

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