Assessing the health impact of interventions for baker's allergy and asthma in supermarket bakeries: a group randomised trial.

PURPOSE: To assess the impact of an intervention for baker's allergy and asthma in supermarket bakeries. METHODS: A group randomised trial conducted in 31 bakeries (n = 337 bakers) that were randomly assigned to one of two intervention groups (n = 244 bakers) and a control group (n = 93 bakers). Health data collected prior to and 1-year after the intervention included information obtained from an ECRHS questionnaire; tests for atopy and serum-specific IgE to cereal flours; fractional exhaled nitric oxide (FeNO). Data from the two intervention groups were combined to form one intervention group for purposes of the statistical analysis. RESULTS: At 1 year of follow-up, the incidence and level of decline of work-related ocular-nasal and chest symptoms, sensitisation status and elevated FeNO (FeNO > 25 ppb) was similar in both intervention and control groups. The mean FeNO difference was also similar across both groups (2.2 ppb vs 1.7 ppb, p = 0.86). In those with FeNO > 25 ppb at baseline, the decline was greater in the intervention compared to control group (16.9 ppb vs 7.7 ppb, p = 0.24). Multivariate logistic regression models (adjusting for smoking, baseline sensitisation to cereal flour, baseline FeNO > 25 ppb) did not demonstrate an appreciable FeNO decline (≥ 10%) in the intervention compared to control group. However, stratification by the presence of work-related ocular-nasal symptoms in bakers at baseline demonstrated a significant FeNO decline (≥ 10%) in the intervention compared to the control group (OR 3.73, CI 1.22-11.42). CONCLUSION: This study demonstrates some evidence of an intervention effect on FeNO 1 year after an intervention, particularly in bakers with work-related ocular-nasal symptoms.

Evaluation of chemical-specific IgG antibodies in male workers from a urethane foam factory.

BACKGROUND: Plastic resins are complex chemicals that contain toluene diisocyanate (TDI) and/or trimellitic anhydride (TMA), which cause occupational allergies (OA), including respiratory allergies. Serum IgGs against TDI and TMA have been suggested as potential markers of the exposure status and as exploring cause of OA. Although TDI-specific IgG has been examined for suspected OA, TMA-specific IgG is not commonly evaluated in a urethane foam factory. This study therefore investigated both TDI- and TMA-specific IgGs in suspected OA patients and to evaluate the usefulness of the measurement of multiple chemical-specific IgG measurement for practical monitoring. METHODS: Blood samples were collected from two male workers who developed respiratory allergies supposedly caused by occupational exposure to TDI and/or TMA for the presence of TDI- and TMA-specific IgGs. In addition, blood samples from 75 male workers from a urethane foam factory, along with 87 male control subjects, were collected in 2014 and tested for the same IgGs in 2014. The presence and levels of TDI- and TMA-specific serum IgGs were measured using dot blot assays. RESULTS: We found that controls had mean concentrations of TDI- and TMA-specific IgGs of 0.98 and 2.10 µg/mL, respectively. In the two workers with respiratory allergies, the TDI-specific IgG concentrations were 15.6 and 9.51 µg/mL, and TMA-specific IgG concentrations were 4.56 and 14.4 µg/mL, which are clearly higher than those in controls. Mean concentrations of TDI- and TMA-specific IgGs in the factory workers were 1.89 and 2.41 µg/mL, respectively, and are significantly higher than those of the controls (P < 0.001 and P < 0.026 for TDI- and TMA-specific IgGs, respectively). CONCLUSION: The workers suspected of OA showed an evidently high level of TDI- and TMA-specific IgG, and these levels in workers at the urethane foam factory were also significantly higher than those in controls. In conclusion, the measurement of TDI- and TMA-specific IgG among workers using plastic resins is helpful to monitor their exposure status.

Granulometry, microbial composition and biological activity of dusts collected in French dairy farms.

BACKGROUND: Dairy working increases the prevalence of lower airway respiratory diseases, especially COPD and asthma. Epidemiological studies have reported that chronic inhalation of organic dusts released during specific daily tasks could represent a major risk factor for development of these pathologies in dairy workers. Knowledge on size, nature and biological activity of such organic dusts remain however limited. OBJECTIVE: To compare size distribution, microbial composition and cellular effects of dusts liberated by the spreading of straw bedding in five French dairy farms located in Brittany. RESULTS: Mechanized distribution of straw bedding generated a cloud of inhalable dusts in the five dairy farms' barns. Thoracic particles having a 3-7.5µm size constituted 58.9-68.3% of these dusts. Analyses of thoracic dusts by next generation sequencing showed that the microbial dust composition differed between the five French farms, although Actinobacteria, Bacteroidetes, Firmicutes and Proteobacteria represent more than 97.5% of the bacterial phyla detected in each sample. Several bacteria genera comprising of human pathogenic species, such as Pseudomonas, Staphylococcus, Thermoactinomyces or Saccharopolyspora were identified. Cladosporium and Alternaria fungal genera, which are potent environmental determinants of respiratory symptoms, were detected in dusts collected in the five farms and their levels reached 15.5-51.1% and 9-24.7% of assignable fungal sequences in each sample, respectively. Finally, all dust samples significantly and strongly increased the expression of the pro-inflammatory TNF-α, IL-1ß, IL-6 and IL-8 cytokines at both mRNA and protein levels in human monocyte-derived macrophages. Their effects were dose-dependent and detectable from 1µg/ml. The intensity of the macrophage responses however differed according to the samples. CONCLUSIONS: Our results strengthen the hypothesis that organic dusts released during the distribution of straw bedding are mainly constituted of thoracic particles which are small enough to deposit on lower bronchial epithelium of dairy farmers and induce inflammation.

Toluene diisocyanate and methylene diphenyl diisocyanate: asthmatic response and cross-reactivity in a mouse model.

Both 2,4-toluene diisocyanate (TDI) and 4,4-methylene diphenyl diisocyanate (MDI) can cause occupational asthma. In this study, we optimized our mouse model of chemical-induced asthma in the C57Bl/6 mice strain using the model agent TDI. Furthermore, we validated MDI in this mouse model and investigated whether cross-reactivity between TDI and MDI is present. On days 1 and 8, C57Bl/6 mice were dermally treated (20 µl/ear) with 3 % MDI, 2 % TDI or the vehicle acetone olive oil (AOO) (3:2). On day 15, they received a single oropharyngeal challenge with 0.04 % MDI, 0.01 % TDI or the vehicle AOO (4:1). One day later, airway hyperreactivity (AHR) and pulmonary inflammation in the bronchoalveolar lavage (BAL) were assessed. Furthermore, total serum IgE levels, lymphocyte subpopulations in auricular lymph nodes and cytokine levels in supernatants of lymphocytes were measured. Both dermal sensitization with TDI or MDI resulted in increased total serum IgE levels along with T and B cell proliferation in the auricular lymph nodes. The auricular lymphocytes showed an increased release of both Th2 and Th1 cytokines. Mice sensitized and challenged with either TDI or MDI showed AHR, along with a predominant neutrophil lung inflammation. Mice sensitized with MDI and challenged with TDI or the other way around showed no AHR, nor BAL inflammation. Both TDI and MDI are able to induce an asthma-like response in this mouse model. However, cross-reactivity between both diisocyanates remained absent.

Proteases in agricultural dust induce lung inflammation through PAR-1 and PAR-2 activation.

Workers exposed to aerosolized dust present in concentrated animal feeding operations (CAFOs) are susceptible to inflammatory lung diseases, such as chronic obstructive pulmonary disease. Extracts of dust collected from hog CAFOs [hog dust extract (HDE)] are potent stimulators of lung inflammatory responses in several model systems. The observation that HDE contains active proteases prompted the present study, which evaluated the role of CAFO dust proteases in lung inflammatory processes and tested whether protease-activated receptors (PARs) are involved in the signaling pathway for these events. We hypothesized that the damaging proinflammatory effect of HDE is due, in part, to the proteolytic activation of PARs, and inhibiting the proteases in HDE or disrupting PAR activation would attenuate HDE-mediated inflammatory indexes in bronchial epithelial cells (BECs), in mouse lung slices in vitro, and in a murine in vivo exposure model. Human BECs and mouse lung slice cultures stimulated with 5% HDE released significantly more of each of the cytokines measured (IL-6, IL-8, TNF-α, keratinocyte-derived chemokine/CXC chemokine ligand 1, and macrophage inflammatory protein-2/CXC chemokine ligand 2) than controls, and these effects were markedly diminished by protease inhibition. Inhibition of PARs also blunted the HDE-induced cytokine release from BECs. In addition, protease depletion inhibited HDE-induced BEC intracellular PKCα and PKCε activation. C57BL/6J mice administered 12.5% HDE intranasally, either once or daily for 3 wk, exhibited increased total cellular and neutrophil influx, bronchial alveolar fluid inflammatory cytokines, lung histopathology, and inflammatory scores compared with mice receiving protease-depleted HDE. These data suggest that proteases in dust from CAFOs are important mediators of lung inflammation, and these proteases and their receptors may provide novel targets for therapeutic intervention in CAFO dust-induced airways disease.

The hapten-atopy hypothesis III: the potential role of airborne chemicals.

One explanation for the large increase in the prevalence of atopic disease in developed countries during the last 50 years is the 'hygiene hypothesis'. This proposes that a reduced exposure to pathogenic microorganisms at a key period(s) during development results in the maintenance or acquisition of an atopic phenotype. Alternatively, or additionally, we have postulated that increased exposure to chemicals generally, and to irritant/haptenic chemicals in particular, during critical windows of maternal pregnancy/early life have also contributed to changes in the prevalence of atopic disease. Having previously reviewed the potential roles of oral and cutaneous exposure to chemicals on the subsequent diagnosis of atopic disease, we here consider possible evidence of a role for exposure to airborne chemicals as a contributory factor in acquired susceptibility to atopic allergy. After controlling for known confounders, five specific maternal occupations during pregnancy have been implicated as being associated with subsequent atopic disease in the offspring. Each of these occupations is characterized by high and persistent exposure to airborne chemicals. High-level exposure to volatile organic compounds in the domestic environment, either during pregnancy or in early life, is also associated with development of childhood atopic disease. Similarly, sustained exposure to airborne chlorinated chemicals from swimming pools during childhood has been associated with the development of atopic allergy. A possible immunological basis for these associations is that exposure to certain airborne chemicals, even at low levels, can result in the delivery of 'danger' signals that, in turn, bias the immune response towards the selective induction or maintenance of preferential T helper 2-type immune responses consistent with the acquisition of allergic sensitization.

Man-made mineral fibers and interstitial lung diseases.

PURPOSE OF REVIEW: Manufactured (artificial) fibers represent an important and continuously growing volume among substitutes to natural fibers. A major proportion of the population in an industrialized society has been, is, or will be in contact with these fibers. The fibrous configuration of asbestos is well recognized as being an important parameter in toxicity, and now that of synthetic fibers is also suspected of inducing serious health effects on the respiratory system. There is an ongoing debate about the actual fibrogenic effect of these man-made mineral fibers (MMMFs) in humans. RECENT FINDINGS: Several case reports have demonstrated the biopersistance of MMMFs in the lung of workers who were exposed to rock wool or fiberglass for long periods of time and were diagnosed with interstitial pulmonary fibrosis. A 20-year follow up also identified refractory ceramic fibers in workers' lung tissue, with significant association between cumulative fiber exposure and radiographic pleural changes. Newly emerging man-made fiber industries appear to induce new types of occupational diseases. SUMMARY: Exposure of workers in MMMFs production plants is correlated to high risk for developing pneumoconiosis. Large epidemiological studies are needed in order to determine dose metrics for risk assessment and management.

Sensitisation to cereal flour allergens is a major determinant of elevated exhaled nitric oxide in bakers.

OBJECTIVE: Various studies of the usefulness of fractional exhaled nitric oxide (FeNO) in occupational settings remain inconclusive. The objective was to investigate the determinants of increased FeNO in bakery workers. METHODS: A cross-sectional study of 424 supermarket bakery workers used a questionnaire and serum specific IgE to wheat, rye and α-amylase. FeNO during the work shift were assessed using a hand-held portable sampling device (NIOX MINO). RESULTS: The median FeNO was 15 ppb, in atopics 21 ppb and current smokers 12 ppb. Increased FeNO was strongly associated with IgE to wheat independent of smoking and atopy status. In the multivariate model, IgE to wheat, current smoking, atopy and age were significantly associated with FeNO. Stratified analysis in a subgroup of atopic non-smokers demonstrated the strongest relationship between FeNO and various clinical endpoint such as wheat (OR=9.43) or rye (OR=11.76) sensitisation, work-related allergic rhinitis (OR=8.13) or asthma (OR=5.44), and probable baker's asthma (OR=6.72). CONCLUSIONS: Sensitisation to cereal flour allergens rather than asthma symptoms is a major determinant of elevated FeNO among bakers. This relationship is modified by atopy and current smoking status.

A stone miner with both silicosis and constrictive pericarditis: case report and review of the literature.

BACKGROUND: The working environment of stone miners has been believed to cause their susceptibility to respiratory diseases. Silicosis is an occupational disease caused by exposure to crystalline silica dust which is marked by inflammation and scarring in the lung. The immune system boosted after the silica invasion led to self-damage and lay the foundation of silicosis pathogenesis. Silicosis coexisting with other diseases in one patient has been reported, however, was not reported to coexist with constrictive pericarditis. We, for the first time, reported a patient with silicosis and constrictive pericarditis and thought the immune response was probably the link between the two. CASE PRESENTATION: A 59-year-old Chinese stone miner complained of chest distress was found to have lung nodules which were found to be silica deposits by biopsy. This patient was also found to have constrictive pericarditis at the same time. Later surgical decortication cured his symptoms. CONCLUSION: We provided the first case having constrictive pericarditis concomitant with silicosis. A probable link between the two diseases was the immune response boosted by the silica deposits.

IgG to various beta-glucans in a human adult population.

BACKGROUND: Fungal ß-(1,3)-glucans are pro-inflammatory agents, and exposures to ß-(1,3)-glucans are associated with respiratory tract symptoms. IgG anti-(1,3)-glucan titers are measured in diagnosis of fungal infections. Although other ß-glucan structures exist, like ß-(1,6)-glucans, little is known about their antigenic or pro-inflammatory properties. We aimed to investigate IgG titers and specificities in human sera against different ß-glucans with varying structures. METHODS: IgG anti-ß-glucan was measured by enzyme immunoassay in a random sample of 40 sera from healthy adults, with a panel of 8 differently structured glucans. In a subsequent larger series, IgG anti-ß-(1,6)-glucan was measured in a random sample of 667 sera from three occupational populations with different organic dust exposures. Possible determinants of IgG anti-ß-(1,6)-glucan titers were explored with linear-regression analysis. RESULTS: We found wide variation in anti-ß-glucan IgG levels. The highest titers were found for pure ß-(1,6)-glucan pustulan. Moderate to strong reactions with other ß-(1,6)-containing structures appeared to be due to cross-reacting anti-ß-(1,6)-glucan antibodies. Surprisingly, the mean IgG anti-ß-(1,6)-glucan titer was significantly lower in agricultural workers - with highest organic dust exposure - than in spray painters and bakery workers. Smoking status was associated with lower IgG anti-ß-(1,6)-glucan titers in all populations. CONCLUSIONS: IgG to ß-(1,3)- and ß-(1,6)-glucans can be found in normal human sera. ß-(1,6)-glucans appear to be much more potent antigens. The health impact of high anti-ß-(1,6)-glucan antibody levels remains unclear and further investigations are needed.

Sensitisation to common allergens and respiratory symptoms in endotoxin exposed workers: a pooled analysis.

OBJECTIVE: To test the hypotheses that current endotoxin exposure is inversely associated with allergic sensitisation and positively associated with non-allergic respiratory diseases in four occupationally exposed populations using a standardised analytical approach. METHODS: Data were pooled from four epidemiological studies including 3883 Dutch and Danish employees in veterinary medicine, agriculture and power plants using biofuel. Endotoxin exposure was estimated by quantitative job-exposure matrices specific for the study populations. Dose-response relationships between exposure, IgE-mediated sensitisation to common allergens and self-reported health symptoms were assessed using logistic regression and generalised additive modelling. Adjustments were made for study, age, sex, atopic predisposition, smoking habit and farm childhood. Heterogeneity was assessed by analysis stratified by study. RESULTS: Current endotoxin exposure was dose-dependently associated with a reduced prevalence of allergic sensitisation (ORs of 0.92, 0.81 and 0.66 for low mediate, high mediate and high exposure) and hay fever (ORs of 1.16, 0.81 and 0.58). Endotoxin exposure was a risk factor for organic dust toxic syndrome, and levels above 100 EU/m(3) significantly increased the risk of chronic bronchitis (p<0.0001). Stratification by farm childhood showed no effect modification except for allergic sensitisation. Only among workers without a farm childhood, endotoxin exposure was inversely associated with allergic sensitisation. Heterogeneity was primarily present for biofuel workers. CONCLUSIONS: Occupational endotoxin exposure has a protective effect on allergic sensitisation and hay fever but increases the risk for organic dust toxic syndrome and chronic bronchitis. Endotoxin's protective effects are most clearly observed among agricultural workers.

Symptoms, spirometry, and serum antibody concentrations among compost workers exposed to organic dust.

Work-related symptoms and diseases of 190 currently exposed compost workers, 59 former compost workers, and 38 nonexposed control subjects were investigated in a cross-sectional study. Using a standardized questionnaire, participants were asked for work-related symptoms, exposures to bioaerosols, atopic diseases, and smoking habits. The subjects underwent a physical examination and a lung function test. In addition, total immunoglobulin (Ig) E, IgE specific to environmental allergens and moulds, and IgG specific to molds and actinomycetes were quantified. Compared to controls, compost workers suffered more often from cough and irritation of the eyes in terms of mucosal membrane irritation (MMI). Former compost workers reported similar work-related complaints, but most MMI symptoms had improved after termination of bioaerosol exposure. In contrast, cough and dyspnea persisted, indicating a chronic process. Lung function parameters of compost workers were within the reference ranges. Nevertheless, forced vital capacity (FVC) was significantly lower than for controls. Specific IgE to environmental allergens and molds was positive in 25.3% and 7.4%, respectively, of currently exposed compost workers. There were no marked differences in IgE and IgG concentrations among the three groups. Compost workers suffered with a higher frequency from cough and MMI symptoms. The findings that MMI symptoms improved in former compost workers after leaving the job confirmed the association with bioaerosol exposure. Further, the reduced FVC may be produced by this exposure. There was no higher frequency of mold sensitization in the group of compost workers compared to controls, which may be an indication of a healthy worker survivor effect.

Systematic review: Progression of beryllium sensitization to chronic beryllium disease.

BACKGROUND: The relevance of beryllium sensitization testing for occupational health practice and prevention is unclear. AIMS: To analyse the natural course of beryllium sensitization and clarify the prognosis following cessation of exposure among sensitized workers. METHODS: An electronic literature search was conducted in PubMed, Embase, Toxline and Cochrane databases supplemented by a manual search. Data abstraction and study quality assessment with adapted guideline checklists were performed independently by three reviewers. Seven studies met the eligibility criteria and were included in the systematic review; however, six of the seven studies were of low methodological quality. RESULTS: A substantial (although not specifically quantifiable) proportion of beryllium-sensitized employees will develop chronic beryllium disease (CBD). To date, it is unknown if cessation of exposure in sensitized workers reduces the progression rate to CBD. CONCLUSIONS: To determine the utility of regular assessments for beryllium sensitization among exposed workers, there is a need for prospective studies. This should include detailed and continuous exposure monitoring, regular tests for beryllium sensitization and a thorough diagnostic evaluation of sensitized workers to confirm or exclude CBD.

Both the variability and level of mouse allergen exposure influence the phenotype of the immune response in workers at a mouse facility.

BACKGROUND: The role of natural aeroallergen exposure in modulating allergen-specific immune responses is not well understood. OBJECTIVE: We sought to examine relationships between mouse allergen exposure and mouse-specific immune responses. METHODS: New employees (n = 179) at a mouse facility underwent repeated assessment of mouse allergen exposure, skin prick tests (SPTs), and measurement of mouse-specific IgG levels. Relationships between the mean level of exposure, variability of exposure (calculated as log deviation), and time to development of immunologic outcomes were examined by using Cox proportional hazards models. RESULTS: By 24 months, 32 (23%) participants had experienced a positive SPT response, and 10 (8%) had mouse-specific IgG4. The incidence of a positive SPT response increased as levels of exposure increased from low to moderate, peaking at 1.2 ng/m³, and decreased beyond this point (P = .04). The more variable the exposure was across visits, the lower the incidence of a positive SPT response (hazard ratio [HR], 0.17; 95% CI, 0.07-0.41). Variability of exposure was an independent predictor of a positive SPT response in a model that included both exposure metrics. In contrast, the incidence of mouse-specific IgG4 increased with increasing levels of mouse allergen exposure (HR, 2.9; 95% CI, 1.4-6.0), and there was evidence of a higher risk of mouse-specific IgG4 with greater variability of exposure (HR, 6.3; 95% CI, 0.4-95.2). CONCLUSION: Both the level and variability of mouse allergen exposure influence the humoral immune response, with specific patterns of exposure associated with specific immunophenotypes. Exposure variability might be a more important predictor of a positive SPT response, whereas the average exposure level might be a more important predictor of mouse-specific IgG4.

Influence of the environment and occupational exposure on the occurrence of Q fever.

Q fever, which is caused by Coxiella bumetii, is a worldwide zoonotic infectious disease and ruminants are the main reservoir for human infections. Humans become infected primarily by inhaling aerosols that are contaminated with C. bumetii. Ingestion (particularly drinking raw milk) and person-to-person transmission are minor routes. Animals shed the bacterium in urine and faeces, and in very high concentrations in birth by-products. The bacterium persists in the environment in a resistant spore-like form which may become airborne and transported long distances by the wind. Q fever is considered primarily an occupational disease of workers in close contact with farm animals or processing their products, however, it may occur also in persons without direct contact. To prevent the introduction and spread of Q fever infection, preventive measures should be implemented including immunisation with currently available vaccines of domestic animals and humans at risk.

Occupational rhinitis in bell pepper greenhouse workers: determinants of leaving work and the effects of subsequent allergen avoidance on health-related quality of life.

BACKGROUND: Avoidance of occupational allergens or reduction in exposure has been advocated as the mainstay of the management of occupational rhinitis. Sparse data to the effect of allergen avoidance are available. OBJECTIVE: To identify factors that may lead to leaving work and to address the effect of subsequent allergen avoidance on quality of life. METHODS: A survey to the prevalence of occupational allergy to bell pepper performed in 1999 comprised 472 employees, of which 254 had work-related rhinitis and 228 completed the Rhinitis-related Quality of Life Questionnaire. After 8-year follow-up in 2007, 91 workers with rhinitis in 1999 were available to fill out the questionnaire again and were used to evaluate the course of nasal disease in terms of perceived severity and impact on daily life. RESULTS: Workers with rhinitis at baseline were more likely to leave their job in bell pepper cultivation for another job (OR = 1.62, 95% CI 0.95-2.75). Among the 91 workers, 58 subjects were still at work, whereas 33 subjects had left work. The subjects who left jobs reported substantial improvement in quality of life. The magnitude of the changes ranged from -0.31 to -1. The effect of quitting work on the mean quality of life score amounted -0.76 ± 0.15. CONCLUSIONS: The current study is the first large longitudinal studies showing that leaving work and subsequent occupational allergen avoidance have a beneficial effect on rhinitis-related quality of life. The study suggests that occupational rhinitis can be a reason to leave work.

Exposure to formaldehyde and its potential human health hazards.

A widely used chemical, formaldehyde is normally present in both indoor and outdoor air. The rapid growth of formaldehyde-related industries in the past two decades reflects the result of its increased use in building materials and other commercial sectors. Consequently, formaldehyde is encountered almost every day from large segments of society due to its various sources. Many governments and agencies around the world have thus issued a series of standards to regulate its exposure in homes, office buildings, workshops, public places, and food. In light of the deleterious properties of formaldehyde, this article provides an overview of its market, regulation standards, and human health effects.

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.

[Evaluation of occupational allergic diseases of the respiratory tract].

The paper presents the basic etiological and pathogenetic aspects of occupational allergic diseases of the respiratory tract, discusses the clinical course, diagnosis, and priorities of the prevention of allergic diseases of the upper airways and bronchopulmonary apparatus from the action of industrial allergens.