Asthma related to workplace dampness and impaired work ability.

PURPOSE: To examine the long-term effects on work ability among patients previously diagnosed with occupational asthma (OA) or work-exacerbated asthma (WEA) or symptoms in relation to workplace dampness. METHODS: A questionnaire follow-up was used to study 1,098 patients (of whom 87 % were female) examined because of a suspected occupational respiratory disease caused by building dampness and mold. Self-rated work ability and early withdrawal from work were the two outcomes of the study. As determinants, we investigated the influence of the asthma diagnosis given in the initial examinations (OA or WEA), the number of persistent indoor air symptoms, and the psychosocial factors at work. RESULTS: With a mean follow-up of 7.8 years, 40 % of the OA patients, under 65 years of age, were outside worklife versus 23 % of the WEA patients and 15 % of the patients with only upper respiratory symptoms at baseline. The diagnosis of OA was associated with a nearly sixfold risk for early withdrawal from work in a comparison with a reference group with upper respiratory symptoms. A perceived poor social climate at work and poor experiences with supervisory co-operation were associated with impaired work ability outcomes. Those with multiple, long-term indoor air symptoms considerably more often perceived their work ability to be poor when compared with those with less significant symptoms. CONCLUSIONS: Adverse work ability outcomes are associated with asthma in relation to workplace dampness. The study raises the need for effective preventive measures in order to help workers with indoor air symptoms sustain their work ability.

Quality of life of patients with asthma related to damp and moldy work environments.

OBJECTIVE: Long-term outcomes of asthma related to exposure to workplace dampness are not well known. The aim of this study was to evaluate the quality of life (QOL) of patients with asthma related to damp and moldy workplaces and characterize factors influencing QOL. METHODS: Using a questionnaire, we followed 1267 patients previously examined for suspected occupational respiratory disease related to exposure to damp and moldy indoor environments. In addition to demographic and other background data, the questionnaire included sections on current employment status, QOL, anxiety and depression, somatization, hypochondria, and asthma medication. We compared the QOL of patients with occupational asthma (OA) with that of patients with work-exacerbated asthma (WEA) or symptoms without asthma. RESULTS: Impaired QOL was found among patients diagnosed with OA when they were compared with patients in corresponding environments with WEA or symptoms only. Not working and greater use of asthma medication were major determinants of worse QOL. Psychological factors did not explain the differences between the groups. CONCLUSIONS: OA induced by exposure to workplace moisture and molds is associated with QOL deterioration. The impairment is related to being unemployed (due to disability, retirement, job loss or other reasons) and the need for medication.

Prolonged exposure to damp and moldy workplaces and new-onset asthma.

PURPOSE: Epidemiological evidence shows that indoor dampness is associated with respiratory symptoms, the aggravation of preexisting asthma, and the development of new-onset asthma. Follow-up studies indicate that symptoms compatible with asthma constitute risk factors for the future development of asthma. The aims of the study were (1) to assess whether asthma-like symptoms (cough, dyspnea, and wheeze) that occur in relation to exposure to damp and moldy work environments lead to the later development of asthma and (2) to assess the importance of continued exposure to indoor dampness and molds at work in the development of asthma. METHODS: We followed 483 patients with asthma-like symptoms related to damp workplaces but without objective evidence of asthma in baseline examinations. The development of asthma and present work conditions were established with the use of a questionnaire 3-12 years later. RESULTS: A total of 62 patients (13%) reported having developed asthma during the study period. Continued exposure to a damp or moldy environment was associated with a more than fourfold increase in the risk of asthma (odds ratio 4.6, 95% confidence interval 1.8-11.6). Working in a non-remediated environment at follow-up was the strongest risk factor for developing asthma. The remediation of damp buildings seemed to be associated with a decrease in the risk of asthma. CONCLUSIONS: The results indicate that exposure at work to dampness and molds is associated with the occurrence of new-onset asthma. Exposed workers suffering from asthma-like symptoms represent a risk group for the development of asthma. The risk appears especially high if the exposure continues. Due to inherent weaknesses of patient series, the findings need corroborative studies.

New-onset adult asthma in relation to damp and moldy workplaces.

OBJECTIVE: Damp and moldy indoor environments aggravate pre-existing asthma. Recent meta-analyses suggest that exposure to such environments may also induce new-onset asthma. We assessed the probability of molds being the cause of asthma in a patient series examined because of respiratory symptoms in relation to workplace dampness and molds. METHODS: Altogether 694 such patients had been clinically assessed between 1995 and 2004. According to their histories, they had all been exposed to molds at work and had suffered from work-related lower respiratory symptoms. The investigations had included specific inhalation challenge (SIC) tests with mold extracts and serial peak expiratory flow (PEF) recordings. Using internationally recommended diagnostic criteria for occupational asthma (OA), we categorized the patients into three groups: probable, possible, and unlikely OA (156, 45, and 475 patients, respectively). The clinical details of 258 patients were analyzed, and their levels of microbial exposure were evaluated. RESULTS: The agreement between the serial PEF recordings and SIC tests (both being either positive or negative) was 56%. In the group of probable OA, mold sensitization was found in 20%. The level of exposure and sensitization to molds was associated with probable OA. At 6 months, the follow-up examinations of 136 patients with probable OA showed that the symptoms were persistent, and no improvement in spirometry was noted despite adequate treatment. Only 58% of the patients had returned to work. CONCLUSIONS: Exposure to damp and moldy workplaces can induce new-onset adult asthma. IgE mediation is a rare mechanism, whereas other mechanisms are unknown.

Occupational rhinitis in damp and moldy workplaces.

BACKGROUND: Numerous studies confirm the association between exposure to indoor air dampness and molds and different health outcomes. Of these, upper respiratory tract problems are the most commonly reported work-related symptoms in damp indoor environments. The aim of this study was to describe a clinically investigated patient series with occupational rhinitis induced by molds. METHODS: Nasal provocation test (NPT) with commercial fungal allergens was performed in 369 patients during 1995-2004 at the Finnish Institute of Occupational Health. Of these, 60 (16%) were positive. In addition to positive NPT, the diagnosis of occupational rhinitis was based on verified exposure to molds, work-related nasal symptoms, and clinical investigations. We wanted to review the patient files of these 60 patients retrospectively, and 56 patients gave their informed consent. RESULTS: The mean age of the patients was 43.7 years (SD +/- 9.5). Fifty (89.3%) patients were women. In 23% of the patients, IgE-mediated allergy to molds could be established. Atopy significantly increased IgE sensitization to molds (OR, 10.3 [95% CI, 2.0-52.5]). The most common mold to induce occupational rhinitis was Aspergillus fumigatus. Exposure time was over 5 years in 63% of the patients. Association between the IgE sensitization to molds and exposure level was statistically significant (Fisher's exact test, p = 0.046). CONCLUSION: This is the first clinically investigated series on occupational rhinitis in relation to a moldy environment. Based on our findings, we conclude that molds growing in conjunction with moisture damages can induce occupational rhinitis. IgE-mediated allergy to molds was not common. Atopy and significant exposure level increased IgE sensitization to molds. zri00508.

Work, unemployment and life satisfaction among patients with diisocyanate induced asthma--a prospective study.

Occupational asthma has been found to be associated with lowered socio-economic outcomes, an increased unemployment rate and a decreased quality of life. The compensation of occupational diseases is comparatively favourable in Finland. Our aim was to follow-up the working status and life satisfaction of patients with diisocyanate-induced asthma in 245 cases diagnosed during 1976-1992. A questionnaire was sent out on average 10 (3-19) yr after the diagnosis to the surviving 235 patients. The questionnaire was validated by re-examining 91 of them clinically, and with spirometry, histamine challenge test and peak flow surveillance. Of the 213 responding patients, 14% were unemployed, and for 50% of them unemployment was caused by asthma. Unemployment was associated with nocturnal asthma symptoms (OR 10.93; CI 2.69-44.452), increased PEF variability (OR 8.46; CI 1.52-46.97) and with the use of short-acting beta-sympathomimetic medication (p=0.045). Satisfaction with life was associated with present working (OR 3.50; CI 1.73-7.06) and with good condition of asthma as assessed by the use of asthma medication (OR 0.49; CI 0.27-0.89) and objective measurements of the asthma condition, e.g. PEF variability (OR 0.21; CI 0.08-0.59). As a conclusion, unemployment was remarkably low as compared with earlier reports and related to the period of simultaneous economic recession. Unemployment, as well as dissatisfaction with life were associated with poor conditions of asthma. Unemployment was associated with improper asthma care favouring the use of short-acting beta-sympathomimetic medication. Proper follow-up of asthma is essential for minimizing the social complaints of occupational asthma, as well as for enhancing life satisfaction.

Prolonged respiratory symptoms caused by thermal degradation products of freons.

OBJECTIVES: The chlorofluorocarbons (CFC) used in refrigeration systems decompose on heating and produce substances that are highly irritating to the airways (eg, chlorine, carbonyl fluoride, and hydrogen fluoride). This study examined persistent respiratory symptoms among several workers exposed to thermal decomposition products of CFC. METHODS: Seven patients with respiratory symptoms caused by inadvertent exposure to thermal decomposition products of CFC in a restaurant kitchen or during refrigerator repair were studied with the use of spirometry, peak flow follow-up, and histamine challenge tests. Three patients also underwent bronchoscopy and bronchoalveolar lavage. RESULTS: In five of the cases, cough or dyspnea lasted longer than 1 month; for three of the five, the symptoms lasted more than 4 years. Three cases showed increased bronchial hyperreactivity, and two of the three had increased diurnal peak flow variation. Three patients fulfilled the criteria for acute irritant-induced asthma or reactive airway dysfunction syndrome. One case exhibited bronchiolitis while, for the other six, the clinical picture was consistent with bronchitis. CONCLUSIONS: The studied cases indicate that the thermal decomposition products of CFC used in refrigerators may cause irritant-induced airway diseases of long duration.

Strain- and blood group-dependent binding of Helicobacter pylori to human gastric MUC5AC glycoforms.

BACKGROUND & AIMS: In the stomach, Helicobacter pylori is found both in the mucus layer and adhering to the gastric epithelium. The aim of this study is to characterize the binding of H. pylori to human gastric mucins. METHODS: H. pylori strains that bind the Lewis(b) (Le(b)) structure (via the BabA adhesin) and/or sialylated structures, along with isogenic adhesion deletion mutants, were used to identify microbe-binding mucins. Gastric mucins from 5 healthy individuals, isolated by density-gradient centrifugation, were investigated for H. pylori binding at neutral pH using a microtiter-based technique. RESULTS: H. pylori strains that express the BabA adhesins were shown to bind to the MUC5AC mucin in individuals expressing the Le(b) antigen. Further fractionation with an ion-exchange chromatography revealed Le(b)-positive MUC5AC glycoforms that differed in their receptor properties for different H. pylori strains. None of the H. pylori strains studied bound to mucins from Le(b)-negative individuals. However, all strains bound to low-density, nonmucin, Le(b)-negative material on top of the gradients. CONCLUSIONS: Binding of H. pylori to human gastric MUC5AC isolated from healthy individuals is BabA dependent and mediated by the Le(b) structure presented by the mucin. However, the BabA adhesins demonstrate strain-dependent preference in binding to MUC5AC glycoforms substituted with Le(b), allowing for great interindividual variability in host-microbe interactions.

Indoor dampness and molds and development of adult-onset asthma: a population-based incident case-control study.

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.

Gastric MUC5AC and MUC6 are large oligomeric mucins that differ in size, glycosylation and tissue distribution.

Gastric MUC5AC and MUC6 mucins were studied using polyclonal antibodies. Immunohistochemistry showed MUC5AC to originate from the surface epithelium, whereas MUC6 was produced by the glands. Mucins from the surface epithelium or glands of corpus and antrum were purified using CsCl/4M guanidinium chloride density-gradient centrifugation. MUC5AC appeared as two distinct populations at 1.4 and 1.3 g/ml, whereas MUC6, which was enriched in the gland tissue, appeared at 1.45 g/ml. Reactivity with antibodies against the Le(b) structure (where Le represents the Lewis antigen) followed the MUC5AC distribution, whereas antibodies against the Le(y) structure and reactivity with the GlcNAc-selective Solanum tuberosum lectin coincided with MUC6, suggesting that the two mucins are glycosylated differently. Rate-zonal centrifugation of whole mucins and reduced subunits showed that both gastric MUC5AC and MUC6 are oligomeric glycoproteins composed of disulphide-bond linked subunits and that oligomeric MUC5AC was apparently smaller than MUC6. A heterogeneous population of 'low-density' MUC5AC mucins, which were smaller than the 'high-density' ones both before and after reduction, reacted with an antibody against a variable number tandem repeat sequence within MUC5AC, suggesting that they represent precursor forms of this mucin. Following ion-exchange HPLC, both MUC5AC and MUC6 appeared as several distinct populations, probably corresponding to 'glycoforms' of the mucins, the most highly charged of which were found in the gland tissue.

N-Acetyltransferase genotypes as modifiers of diisocyanate exposure-associated asthma risk.

We observed previously that polymorphisms in glutathione S-transferase (GST) genes modified allergic responses to diisocyanate exposure. Here, we extended the study to examine the possible role of N-acetyltransferase (NAT) genotypes in the development of diisocyanate-induced ill effects, both separately and in combination with the previously examined GSTM1, GSTM3, GSTP1 and GSTT1 genotypes. The study population comprised 182 diisocyanate-exposed workers, 109 of whom were diagnosed with diisocyanate-induced asthma and 73 of whom had no symptoms of asthma. The diisocyanates to which the workers had been exposed to were diphenylmethane diisocyanate (MDI), hexamethylene diisocyanate (HDI) and toluene diisocyanate (TDI). The NAT2 genotype did not have any significant effect on the risk of developing asthma, but the putative slow acetylator NAT1 genotypes posed a 2.54-fold risk of diisocyanate-induced asthma (95% confidence interval [CI] 1.32 to 4.91). The effect of the NAT1 genotype was especially marked for workers exposed to TDI, among whom the NAT1 slow acetylator genotypes posed a 7.77-fold risk of asthma (95% CI 1.18 to 51.6). Statistically significant increases in asthma risk were also observed among the whole study population for the concurrent presence of the GSTM1 null genotype and either NAT1 (odds ratio [OR] 4.53, 95% CI 1.76 to 11.6) or NAT2 (OR 3.12, 95% CI 1.11 to 8.78) slow acetylator genotypes, and of NAT1 and NAT2 slow acetylator genotypes (OR 4.20, 95% CI 1.51 to 11.6). The results suggest for the first time that in addition to GSTs, the NATs play an important role in inception of asthmatic reactions related to occupational exposure to diisocyanates.