Abstract
Immunoglobulin G (IgG) antibodies against microbes related to indoor dampness problems have been used as potential biomarkers of fungal exposure in clinical investigations. There is limited information on their relation to asthma. We conducted a population-based incident case–control study to assess the risk of asthma in relation to specific IgG antibodies to eight dampness-related microbes: Aspergillus fumigatus, A. versicolor, Cladosporium cladosporioides, Fusarium oxysporum, Sporobolomyces salmonicolor, Stachybotrys chartarum, Streptomyces albus and Trichoderma citrinoviride. We recruited systematically all new cases of asthma during a 2·5-year study period and randomly selected controls from a source population of adults 21–63 years of age 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 selected randomly from the source population. IgG antibodies were analysed with ELISA. An increased risk of developing asthma in adulthood was significantly related to IgG antibodies to T. citrinoviride, but not to the other moulds. There was no evidence of a dose–response relation between the IgG antibody level and the risk of asthma. T. citrinoviride may play a role in the aetiology of adult-onset asthma or serve as an indicator of other causal factors.
Keywords: asthma, moulds, work environment, immunology, case–control
INTRODUCTION
Fungi are eukaryotic microorganisms that colonize dead organic materials in outdoor and indoor environments [1,2]. The species that are able to colonize indoor environments can utilize nutritional sources available in indoor materials, and moisture is the most important factor controlling fungal growth [1,2]. Associations between immunoglobulin G (IgG) antibodies against moulds and occurrence of allergic alveolitis have been found among farmers, and measurement of IgG antibodies as markers of exposure is recommended in investigations of allergic alveolitis [3,4]. Recently, IgG antibodies against microbes related to indoor dampness problems have been used as potential biomarkers of microbe exposure also in clinical investigations of asthma. Studies among farmers, cork workers, malt workers, tobacco workers and wood trimmers have suggested that levels of specific IgG antibodies in serum are related to the exposure level to mould spores and to the daily hours of exposure [4]. In a study from Finland, 92% of 73 subjects with possible exposure to fungus in buildings in which they were living or working had detectable IgG antibodies to Aspergillus versicolor [5]. In addition, 74% of them had antibodies to A. fumigatus. However, little is known about the importance of IgG antibodies against moulds in the context of clinical diseases other than allergic alveolitis and allergic bronchopulmonary aspergillosis [4,6].
We carried out a population-based case–control study of incident asthma among a working-age population, the diagnosis being verified with clinical examinations. We found that occurrence of visible mould and/or mould odour in the workplace was related to the development of new asthma, with an adjusted odds ratio (OR) of 1·54 (95% confidence interval (CI) 1·01–2·32) [7]. Exposure assessment was based on questionnaire-reported occurrence of water damages, damp stains on indoor surfaces, visible mould and mould odour in the workplace or at home. In addition, we collected serum samples of study subjects and analysed IgG antibodies against a panel of eight microbes that have been associated with indoor dampness problems. IgG antibodies against these microbes have been applied commonly in Finland as biomarkers of exposure in clinical investigations of asthma. The aim of this part of the study was to evaluate the relations between IgG antibodies against these eight specific dampness-related microbes and the development of asthma in adulthood.
METHODS
Study design
This study was a population-based incident case–control study. The source population consisted of adults 21–63 years of age living in the Pirkanmaa Hospital District, a geographically defined administrative area in South Finland with a population of 440913 inhabitants (in 1997). The ethics committees of the Finnish Institute of Occupational Health and the Tampere University Hospital approved the study.
Definition and selection of cases
We recruited systematically all the new cases of asthma, first in the city of Tampere beginning on 15 September 1997, and from 10 March 1998 to 31 March 2000 in the whole Pirkanmaa Hospital District. Patients were recruited at all health-care facilities diagnosing asthma, including the Department of Pulmonary Medicine at the Tampere University Hospital, offices of the private-practising pulmonary physicians in the region as well as public health-care centres. As an additional route of case selection, the National Social Insurance Institution of Finland invited all patients, whose reimbursement rights for asthma medication began for the first time during the period 1 September 1997 to 1 May 1999, and who had not yet participated.
The diagnostic criteria applied for asthma are given in Table 1. The diagnostic procedures corresponded to the recommendations of the Asthma Program in Finland [8]. At the Tampere University Hospital, cases were recruited at their first visit due to suspected asthma and the diagnosis was verified in clinical examinations. At the other health-care facilities, cases were recruited immediately when the asthma diagnosis was verified. The National Social Insurance Institution invited the cases 6 months to 2 years after their diagnosis was established. For these patients, the date and criteria of the asthma diagnosis were confirmed from their medical records so that the diagnosis of asthmatics included in our study fulfilled our criteria. Eligible subjects were invited to participate in the study by their physician or through a letter sent by the National Social Insurance Institution. The medical records of all asthma cases were checked and only those with no previous history of diagnosed asthma or long-term use of asthma medication were included in the study. All the confirmed cases of asthma fulfilling the general eligibility criteria were selected as cases. A total of 362 cases (response rate 90%) participated through the health-care system and 159 cases through the National Social Insurance Institution (response rate 78%), totalling 521 cases. Among these, 490 cases (94%) gave a serum sample for IgG antibody analyses. This sample was given immediately after they were recruited.
Table 1.
Diagnostic criteria for asthma
| 1 A history of at least one asthma-like symptom: prolonged cough, wheezing, attacks of or exercise-induced dyspnoea, or nocturnal cough orwheezing and |
| 2 Demonstration of reversibility in airways obstruction in lung function investigations [8]: |
| Significant improvement in response to short-acting bronchodilating medication in a bronchodilator test. The criteria for significant changes were: |
| FEV1: ≥15% |
| FVC: ≥15% |
| PEF: ≥23% |
| and/or |
| ≥20% daily variation and/or ≥15% improvement2 in response to short-acting bronchodilating medication during at least 2 days in a 2-weekdiurnal PEF follow-up |
| and/or |
| Significant improvement in spirometric lung function (for percentage criteria see above) and/or ≥20% improvement in the average PEF level in response to a 2-week oral steroid treatment |
FEV1 = forced expiratory volume in one second, 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.
Selection of controls
The controls were drawn randomly from the source population using the national population registry, which has full coverage of the population. The general eligibility criteria were applied for controls. Recruitment of controls took place at regular intervals throughout the study period. The response rate was 67% of the total invited population or 80% of those who had a telephone number in the Pirkanmaa area. After excluding controls with previous or current asthma (n = 76) and people who were older than 63 years (n = 6) or who had returned an incomplete questionnaire (n = 2), our study population included 932 controls. A total of 668 controls (72%) gave a serum sample for IgG antibody analyses.
Measurement methods
Questionnaire
The self-administered questionnaire, modified from the Helsinki Office Environment Study questionnaire [9,10] to be used in a general population, included six sections: (1) personal characteristics, (2) health information, (3) active smoking and environmental tobacco smoke (ETS) exposure, (4) occupation and work environment, (5) home environment and (6) dietary questions.
Lung function measurements
The lung function protocol included baseline spirometry accompanied by bronchodilation test and performed according to the guidelines by the American Thoracic Society [11], a 2-week diurnal peak expiratory flow (PEF) follow-up and a 2-week steroid treatment trial with PEF follow-up if the other diagnostic tests were negative.
IgG antibody analyses
After the cases and controls had given an informed consent, they gave serum samples at the laboratories of the Centre for Laboratory Medicine, Tampere University Hospital. Serum was separated by centrifugation and stored at −20°C before shipping to the Kuopio Regional Institute of Occupational Health for IgG antibody analyses.
Based on previous literature on the occurrence of microbes in water-damaged buildings [12,13] and previous clinical practice we chose a panel of eight dampness-related microbes and analysed IgG antibodies to these with an enzyme-linked immunosorbent assay (ELISA). The microbes were: Aspergillus fumigatus (mould), A. versicolor (mould), Cladosporium cladosporioides (mould), Fusarium oxysporum (mould), Sporobolomyces salmonicolor (yeast), Stachybotrys chartarum (mould), Streptomyces albus (actinomycete) and Trichoderma citrinoviride (mould).
Intracellular antigens for the antibody assay were prepared from microbial cultures and Centraalbureau voor Schimmelcultures from the Netherlands verified the taxonomic identification of fungi. The selected microbes were grown on agar plates at +25°C. The purity of the fungal isolates was verified before transferring them into peptone broth (2% malt extract, 1% mycological peptone, 4% glucose in sterile water). After incubation for 7 days, the cultures were autoclaved and separated from the fluid by filtration or by centrifugation. The cultures were washed with phosphate-buffered saline (PBS), homogenized and treated by ultrasonic treatment. The homogenates were centrifuged for 30 min at 15000 r.p.m. After filtration through a filter of pore size 0·45 μm, the supernatants were stored at −70°C before use as antigens. The working dilution of antigens was determined from the titration curves for each microbe separately by using IgG positive sera diluted 1:100.
In the ELISA [5], the microtitre plates (Nunc Immuno Plate, Denmark) were coated with 200 μl/well of the antigen extract in PBS (pH 7·4), incubated at +37°C for 6 h, and then washed three times with deionized water. Serum samples diluted 1:100 in 10% FBS (10% fetal bovine serum in PBS) were added in a volume of 200 μl/well and the plates were incubated at + 37°C for 2 h. After washing the wells twice with 0·05% Tween-20 in PBS and once with deionized water, alkaline phosphatase conjugated antihuman IgG (Dako, Glostrup, Denmark) in 10% FBS was added at 200 μl/well at a dilution of 1:400 and incubated for 2h at +37°C. The wells were washed as previously and incubated with the substrate solution, 1 mg/ml p-nitrophenylphosphate (Sigma, St Louis, MO, USA) in diethanolamine-MgCl2 buffer (Reagena, Kuopio, Finland), 200 μl/well at +37°C for 30 min. The enzyme reaction was stopped with 100 μl/well of 2m NaOH, and the absorbances were measured at a wavelength of 405 nm with a spectrophotometer (Labsystems Multiskan MCC/340, Helsinki, Finland). The absorbance of the test serum was given as a percentage of absorbance of a pooled positive control serum combining individual sera of 357 adults. These positive control sera were chosen based on high IgG antibody levels for one microbe at a time. We used this pooled control serum of known positive individual sera because there are no international standardized species-specific control sera available. This method was used to avoid slight differences in the technique applied at different times of determinations.
Statistical methods
We used exposure odds ratio (OR) to quantify the relations between IgG antibody levels to specific microbes and the outcome. The lowest quartile of antibody levels was used as the reference. We estimated adjusted OR in logistic regression analysis. Gender, age, parental atopy or asthma, education (as an indicator of socio-economic status), personal smoking, exposure to environmental tobacco smoke, any history of pets in the home and self-reported occupational exposure to sensitizers, dusts or fumes were used as covariates. In additional analyses we adjusted for IgG antibody levels to other microbes to also evaluate the independent effect of IgG antibodies to each specific microbe.
RESULTS
Characteristics and IgG antibody levels of cases and controls
IgG antibodies were analysed in 490 cases (94% of all cases) and 668 controls (72% of all controls). The characteristics of these cases and controls are presented in Table 2. A larger proportion of cases than controls were women, young, current smokers, exposed to environmental tobacco smoke and to pets, had lower education and reported a history of parental allergic diseases. The characteristics of those with IgG antibody analyses were similar to the total study population [7]. The distributions of IgG antibodies to the eight microbes are shown in Table 3.
Table 2.
Characteristics of the study population
| Cases | Controls | |||
|---|---|---|---|---|
| Characteristic | N | % | N | % |
| Total | 490 | 668 | ||
| Gender | ||||
| Male | 162 | 33·1 | 298 | 44·6 |
| Female | 328 | 66·9 | 370 | 55·4 |
| Age (years) | ||||
| 21–29 | 102 | 20·8 | 85 | 12·7 |
| 30–39 | 100 | 20·4 | 163 | 24·4 |
| 40–49 | 121 | 24·7 | 194 | 29·0 |
| 50–59 | 129 | 26·3 | 173 | 25·9 |
| 60–63 | 38 | 7·8 | 53 | 7·9 |
| Parental atopy and/or asthma | 172 | 35·1 | 150 | 22·5 |
| Education1 | ||||
| No voc. schooling | 99 | 20·3 | 106 | 15·9 |
| Vocational course | 82 | 16·8 | 72 | 10·8 |
| Vocational institution | 141 | 28·9 | 188 | 28·2 |
| College-level education | 108 | 22·1 | 200 | 30·0 |
| University or corresponding | 58 | 11·9 | 100 | 15·0 |
| Smoking2 | ||||
| No | 225 | 46·2 | 348 | 52·2 |
| Ex | 127 | 26·1 | 156 | 23·4 |
| Current | 135 | 27·7 | 163 | 24·4 |
| ETS3 | ||||
| In the workplace | 83 | 16·9 | 92 | 13·8 |
| In the home | 29 | 5·9 | 38 | 5·7 |
| Pets at home4 | ||||
| Sometimes | 345 | 73·5 | 432 | 71·1 |
| Any work exposure | 297 | 60·6 | 429 | 64·2 |
Information on education was missing for four subjects.
Information on smoking was missing for four subjects.
ETS = environmental tobacco smoke.
Self-reported exposure to sensitizers, dusts and/or fumes, except for exposure to moulds.
Table 3.
The risk of asthma in relation to specific IgG antibody levels
| Crude | Adjusted | Adjusted | ||||||
|---|---|---|---|---|---|---|---|---|
| Cases N = 490 % | Controls N = 668 % | OR | 95% CI | OR1 | 95% CI | OR2 | 95% CI | |
| Aspergillus fumigatus | ||||||||
| First quartile | 26·9 | 23·5 | 1·00 | 1·00 | 1·00 | |||
| Second quartile | 25·1 | 25·0 | 0·88 | 0·63–1·22 | 0·82 | 0·58–1·16 | 0·83 | 0·56–1·22 |
| Third quartile | 23·1 | 26·2 | 0·77 | 0·55–1·07 | 0·71 | 0·50–1·00 | 0·73 | 0·48–1·10 |
| Fourth quartile | 24·9 | 25·3 | 0·86 | 0·62–1·19 | 0·72 | 0·50–1·01 | 0·82 | 0·52–1·29 |
| Aspergillus versicolor | ||||||||
| First quartile | 25·9 | 24·2 | 1·00 | 1·00 | 1·00 | |||
| Second quartile | 26·3 | 24·1 | 1·02 | 0·74–1·42 | 1·01 | 0·71–1·42 | 1·22 | 0·81–1·84 |
| Third quartile | 23·1 | 25·8 | 0·84 | 0·60–1·17 | 0·77 | 0·54–1·10 | 1·01 | 0·64–1·59 |
| Fourth quartile | 24·7 | 25·9 | 0·89 | 0·64–1·24 | 0·80 | 0·56–1·13 | 1·05 | 0·65–1·70 |
| Cladosporium cladosporioides | ||||||||
| First quartile | 26·5 | 23·8 | 1·00 | 1·00 | 1·00 | |||
| Second quartile | 25·1 | 25·0 | 0·90 | 0·65–1·25 | 0·89 | 0·63–1·26 | 0·95 | 0·66–1·38 |
| Third quartile | 23·1 | 26·0 | 0·79 | 0·57–1·11 | 0·80 | 0·56–1·13 | 0·86 | 0·58–1·26 |
| Fourth quartile | 25·3 | 25·2 | 0·90 | 0·65–1·25 | 0·76 | 0·54–1·09 | 0·86 | 0·56–1·31 |
| Fusarium oxysporum | ||||||||
| First quartile | 25·1 | 24·7 | 1·00 | 1·00 | 1·00 | |||
| Second quartile | 22·1 | 27·4 | 0·79 | 0·57–1·11 | 0·80 | 0·56–1·13 | 0·84 | 0·58–1·20 |
| Third quartile | 26·3 | 24·0 | 1·08 | 0·78–1·50 | 1·07 | 0·76–1·52 | 1·17 | 0·82–1·68 |
| Fourth quartile | 26·5 | 23·9 | 1·09 | 0·78–1·52 | 1·08 | 0·77–1·53 | 1·18 | 0·82–1·70 |
| Sporobolomyces salmonicolor | ||||||||
| First quartile | 25·3 | 24·7 | 1·00 | 1·00 | 1·00 | |||
| Second quartile | 25·5 | 24·7 | 1·01 | 0·73–1·40 | 0·95 | 0·67–1·34 | 0·98 | 0·68–1·43 |
| Third quartile | 24·7 | 25·1 | 0·96 | 0·69–1·33 | 0·95 | 0·67–1·34 | 1·03 | 0·70–1·53 |
| Fourth quartile | 24·5 | 25·5 | 0·94 | 0·68–1·31 | 0·89 | 0·63–1·26 | 1·00 | 0·64–1·58 |
| Stachybotrys chartarum | ||||||||
| First quartile | 27·3 | 23·2 | 1·00 | 1·00 | 1·00 | |||
| Second quartile | 23·7 | 25·8 | 0·78 | 0·56–1·09 | 0·77 | 0·54–1·08 | 0·80 | 0·55–1·16 |
| Third quartile | 24·3 | 25·8 | 0·80 | 0·58–1·11 | 0·76 | 0·54–1·08 | 0·76 | 0·51–1·12 |
| Fourth quartile | 24·7 | 25·2 | 0·83 | 0·60–1·15 | 0·77 | 0·54–1·08 | 0·81 | 0·52–1·27 |
| Streptomyces albus | ||||||||
| First quartile | 28·4 | 22·5 | 1·00 | 1·00 | 1·00 | |||
| Second quartile | 24·3 | 25·6 | 0·75 | 0·54–1·04 | 0·72 | 0·51–1·01 | 0·71 | 0·49–1·02 |
| Third quartile | 24·3 | 25·4 | 0·76 | 0·54–1·05 | 0·71 | 0·50–1·00 | 0·69 | 0·48–1·01 |
| Fourth quartile | 23·0 | 26·5 | 0·69 | 0·50–0·96 | 0·63 | 0·44–0·89 | 0·64 | 0·43–0·95 |
| Trichoderma citrinoviride | ||||||||
| First quartile | 23·0 | 26·4 | 1·00 | 1·00 | 1·00 | |||
| Second quartile | 27·8 | 23·0 | 1·38 | 0·99–1·91 | 1·39 | 0·98–1·96 | 1·62 | 1·12–2·35 |
| Third quartile | 25·7 | 24·4 | 1·20 | 0·86–1·68 | 1·26 | 0·89–1·78 | 1·59 | 1·07–2·34 |
| Fourth quartile | 23·5 | 26·2 | 1·02 | 0·73–1·43 | 1·06 | 0·74–1·50 | 1·38 | 0·90–2·12 |
Adjusted for sex, age, parental atopy, education, smoking, environmental tobacco smoke (ETS), pets, occupational exposures, working indoors.
Adjusted for sex, age, parental atopy, education, smoking, ETS, pets, occupational exposures, working indoors and other specific IgGs.
IgG antibody levels and the risk of asthma
Table 3 shows the crude and adjusted ORs of asthma and 95% confidence intervals (95% CI) for quartiles of IgG antibody levels to the eight microbes. OR was increased in relation to IgG antibodies against T. citrinoviride, but no evidence of dose–response relation was observed between the IgG antibody level and the risk of asthma. When adjusted for covariates, including IgG antibodies against the other microbes, the ORs for the quartiles of T. citrinoviride IgG antibodies were 1·62 (P = 0·010), 1·59 (P = 0·021) and 1·38 (P = 0·137), respectively. IgG antibody levels to other microbes studied were not associated with the development of asthma in adults.
DISCUSSION
We evaluated specific IgG antibodies to eight microbes that have been associated with indoor dampness problems as biomarkers of exposure. Antibodies to T. citrinoviride were related to an increased risk of asthma developing in adulthood, but there was no evidence of a dose–response relation between the level of antibodies and the risk of asthma. IgG antibodies against other microbes studied were not related to the risk of asthma.
The importance of IgG antibodies against microbes in the context of clinical diseases other than allergic alveolitis and allergic bronchopulmonary aspergillosis has been unclear, although they have been used as biomarkers of exposure to dampness-related microbes also in clinical investigations of asthma. The mechanisms by which such microbes may induce asthma are not well understood. Several possible mechanisms have been suggested, including IgE-mediated hypersensitivity reactions, toxic reactions due to mycotoxins and irritative reactions due to volatile organic compounds emitted by microbes (MVOC) [14,15]. It is likely that different species have their influence by different mechanisms. The microbial growth in indoor environments is a dynamic process depending on environmental conditions, such as humidity, temperature and availability of nutrition, and the main species may differ over time. We selected our panel of eight microbes on the basis of the best current knowledge on occurrence of microbes in water-damaged buildings, but it is possible that the microbes chosen are not the most relevant ones for health effects. Moreover, interpretation of IgG antibodies as biomarkers of exposure is problematic, because such antibodies last in the blood for months and even for years [4]. Thus, it is not possible to identify where and when the person has been exposed to the microbe in question. In addition, it is not known to what extent IgG levels reflect the magnitude of exposure.
The association between increased concentrations of IgG antibodies to T. citrinoviride and the risk of asthma is consistent with but does not necessarily indicate a causal relation between exposure to this species and the development of asthma. For example, it is possible that this species is a marker of other fungi that are more relevant for health effects. In addition, multiple comparisons with eight microbes increase the likelihood of finding a significant relation. The relations between different IgG antibody concentrations of T. citrinoviride and asthma were increased slightly before adjustment was made for the other specific IgGs, but the relations became stronger and statistically significant after the adjustment. This suggests that the other IgGs had obscured the associations with asthma in the analyses without adjustment. Because we chose the microbes on the basis of their common occurrence in buildings with water damages, it is likely that many subjects have been exposed to several of them, and adjustment for the other specific IgGs was needed to address the independent effect of each specific microbe. T. citrinoviride has been detected commonly in water damaged buildings [16] and it requires a high water content for growth, and has been isolated mainly from wood and insulation materials [17]. Some characteristics of T. citrinoviride suggest that this fungus could induce inflammatory reactions in the airways. The diameter of its spores is frequently smaller than 3·5 μm [17], so they can reach small airways. Allergenic properties of T. citrinoviride are not well known, but some Trichoderma species have been found to be allergenic [18]. They produce mycotoxins, including trichothecenes, gliotoxin, cyclopentane derivatives and peptaibols [14,16]. When growing, they may also produce different types of MVOCs [19,20].
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 through the National Social Insurance Institution (response rate 78%). This Institute covers the whole Finnish population and its medication files have almost a full coverage of asthmatics that fulfil the diagnostic criteria required for reimbursement in Finland. The response rate among the control population was also relatively high. A total of 94% of cases and 72% of controls provided a serum sample for IgG analyses. The characteristics of these subjects were essentially similar to those of the total study population and any major selection bias is unlikely in our study.
The use of IgG antibodies to microbes as biomarkers of exposure provides an objective exposure assessment method not vulnerable to information bias. On the other hand, there is the problem of how to identify species relevant for health effects. Defining asthma on the basis of objective clinical findings eliminates information bias concerning the outcome.
Individual characteristics, such as smoking and age, affect a person's tendency to produce IgG antibodies [4,21]. On the other hand, personal atopy does not seem to influence this production [22]. We were able to adjust for an extensive number of potential confounders in logistic regression analysis.
Synthesis with previous knowledge
We are not aware of any previous epidemiological study published on the relations between IgG antibodies to indoor dampness problem-related microbes and development of asthma. A case report has been published recently including 14 people employed by a military hospital in Finland with severe water and mould damage [23]. Four of the employees had asthma verified in an inhalation provocation test with S. salmonicolor, a species that was found in indoor air sampling of the building. All four subjects had increased IgG antibody concentrations against this yeast. However, the study design did not include any control population and, thus, the study does not allow evaluation of potential risk associated with such antibodies. A study of a problem office building in the United States included 47 office workers from areas with elevated airborne fungal (mainly Penicillium) concentrations and 44 office workers from areas with low airborne fungal exposure [24]. A total of 67% of subjects had high IgG antibody levels to at least one of 14 fungal genera, but no significant differences were detected in IgG antibody levels between the workers of the two areas. High IgG antibody levels to Aspergillus were associated with ‘building-related’ nasal and atopic symptoms (ORs 4·8 and 6·2, respectively). On the other hand, high IgG antibody levels to Penicillium were inversely associated with ‘building-related’ cough (OR 0·26). IgG antibodies against Trichoderma were not analysed in this study.
A recent cross-sectional study from Germany evaluated associations between IgG antibodies against six fungi and four actinomycetes and occurrence of health complaints among 58 compost workers, 53 biowaste collectors and 40 control subjects [25]. Increased IgG antibodies to moulds and/or actinomycetes were related to diseases of airways, including mucous membrane irritation, tracheobronchitis and sinusitis, and to skin diseases among compost workers. Occurrence of atopic diseases was lower among compost workers compared to the other two groups, and the authors suggested selection bias (i.e. healthy worker effect) as an explanation for this.
Concluding remarks
The present results suggest that exposure to T. citrinoviride, as measured by IgG antibody levels, is related to the development of new asthma in adulthood. Specific IgG antibodies against seven other indoor dampness-related microbes (A. fumigatus, A. versicolor, C. cladosporioides, F. oxysporum, S. salmonicolor, S. chartarum and Strep. albus) were not associated with the risk of asthma in our study.
Acknowledgments
The authors would like to thank our research nurses Ms Leena Yrjänheikki, Marika Soukkanen and Marita Aalto, as well as all the physicians and nurses who participated in recruiting the study subjects at the Tampere University Hospital, health-care centres and private practices. The authors also thank the laboratory staff of the Kuopio Regional Institute of Occupational Health for their assistance with serum IgG antibody analyses. We would also like to thank the National Social Insurance Institution of Finland for providing us the additional route of case recruitment. This study was funded by the Ministry of Social Affairs and Health of Finland and the Finnish Work Environment Fund.
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