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Background: Asthma is one of the most prevalent chronic respiratory diseases. Despite increased investment in treatment, little progress has been made in the early recognition and treatment of asthma exacerbations over the last decade. Nocturnal cough monitoring may provide an opportunity to identify patients at risk for imminent exacerbations. Recently developed approaches enable smartphone-based cough monitoring. These approaches, however, have not undergone longitudinal overnight testing nor have they been specifically evaluated in the context of asthma. Also, the problem of distinguishing partner coughs from patient coughs when two or more people are sleeping in the same room using contact-free audio recordings remains unsolved., Objective: The objective of this study was to evaluate the automatic recognition and segmentation of nocturnal asthmatic coughs and cough epochs in smartphone-based audio recordings that were collected in the field. We also aimed to distinguish partner coughs from patient coughs in contact-free audio recordings by classifying coughs based on sex., Methods: We used a convolutional neural network model that we had developed in previous work for automated cough recognition. We further used techniques (such as ensemble learning, minibatch balancing, and thresholding) to address the imbalance in the data set. We evaluated the classifier in a classification task and a segmentation task. The cough-recognition classifier served as the basis for the cough-segmentation classifier from continuous audio recordings. We compared automated cough and cough-epoch counts to human-annotated cough and cough-epoch counts. We employed Gaussian mixture models to build a classifier for cough and cough-epoch signals based on sex., Results: We recorded audio data from 94 adults with asthma (overall: mean 43 years; SD 16 years; female: 54/94, 57%; male 40/94, 43%). Audio data were recorded by each participant in their everyday environment using a smartphone placed next to their bed; recordings were made over a period of 28 nights. Out of 704,697 sounds, we identified 30,304 sounds as coughs. A total of 26,166 coughs occurred without a 2-second pause between coughs, yielding 8238 cough epochs. The ensemble classifier performed well with a Matthews correlation coefficient of 92% in a pure classification task and achieved comparable cough counts to that of human annotators in the segmentation of coughing. The count difference between automated and human-annotated coughs was a mean -0.1 (95% CI -12.11, 11.91) coughs. The count difference between automated and human-annotated cough epochs was a mean 0.24 (95% CI -3.67, 4.15) cough epochs. The Gaussian mixture model cough epoch-based sex classification performed best yielding an accuracy of 83%., Conclusions: Our study showed longitudinal nocturnal cough and cough-epoch recognition from nightly recorded smartphone-based audio from adults with asthma. The model distinguishes partner cough from patient cough in contact-free recordings by identifying cough and cough-epoch signals that correspond to the sex of the patient. This research represents a step towards enabling passive and scalable cough monitoring for adults with asthma., (©Filipe Barata, Peter Tinschert, Frank Rassouli, Claudia Steurer-Stey, Elgar Fleisch, Milo Alan Puhan, Martin Brutsche, David Kotz, Tobias Kowatsch. Originally published in the Journal of Medical Internet Research (http://www.jmir.org), 14.07.2020.)

Introduction: Nocturnal cough is a burdensome asthma symptom. However, knowledge about the prevalence of nocturnal cough in asthma is limited. Furthermore, prior research has shown that nocturnal cough and impaired sleep quality are associated with asthma control, but the association between these two symptoms remains unclear. This study further investigates the potential of these symptoms as markers for asthma control and the accuracy of automated, smartphone-based passive monitoring for nocturnal cough detection and sleep quality assessment., Methods and Analysis: The study is a multicentre, longitudinal observational study with two stages. Sensor and questionnaire data of 94 individuals with asthma will be recorded for 28 nights by means of a smartphone. On the first and the last study day, a participant's asthma will be clinically assessed, including spirometry and fractionated exhaled nitric oxide levels. Asthma control will be assessed by the Asthma Control Test and sleep quality by means of the Pittsburgh Sleep Quality Index. In addition, nocturnal coughs from smartphone microphone recordings will be labelled and counted by human annotators. Relatively unrestrictive eligibility criteria for study participation are set to support external validity of study results. Analysis of the first stage is concerned with the prevalence and trends of nocturnal cough and the accuracies of smartphone-based automated detection of nocturnal cough and sleep quality. In the second stage, patient-reported asthma control will be predicted in a mixed effects regression model with nocturnal cough frequencies and sleep quality of past nights as the main predictors., Ethics and Dissemination: The study was reviewed and approved by the ethics commission responsible for research involving humans in eastern Switzerland (BASEC ID: 2017-01872). All study data will be anonymised on study termination. Results will be published in medical and technical peer-reviewed journals., Trial Registration Number: NCT03635710; Pre-results., Competing Interests: Competing interests: PT, FB, EF and TK are affiliated with the Center for Digital Health Interventions (www.c4dhi.org), a joint initiative of the Department of Management, Technology and Economics at ETH Zurich and the Institute of Technology Management at the University of St. Gallen, which is funded in part by the Swiss health insurer CSS. EF and TK are also cofounders of Pathmate Technologies, a university spin-off company that creates and delivers digital clinical pathways and has used the open source MobileCoach platform for that purpose, too. However, Pathmate Technologies is not involved in the study app described in this paper., (© Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Aberrant expression of small noncoding RNAs (sncRNAs), microRNAs (miRNAs) and PIWI-interacting RNAs (piRNAs) in particular, define several pathologic processes. Asthma is characterized by airway hyperreactivity, chronic inflammation, and airway wall remodeling. Asthma-specific miRNA profiles were reported for bronchial epithelial cells, whereas sncRNA expression in asthmatic bronchial smooth muscle (BSM) cells is almost completely unexplored., Objective: We sought to determine whether the primary BSM sncRNA expression profile is altered in asthmatic patients and identify targets of differentially expressed sncRNAs., Methods: Small RNA sequencing was used for sncRNA profiling in BSM cells (from 8 asthmatic and 6 nonasthmatic subjects). sncRNA identification and differential expression analysis was performed with iMir software. Experimentally validated miRNA targets were identified by using Ingenuity Pathway Analysis, and putative piRNA targets were identified by using miRanda software., Results: BSM cells from asthmatic patients showed abnormal expression of 32 sncRNAs (26 miRNAs, 5 piRNAs, and 1 small nucleolar RNA). Target prediction for deregulated miRNAs and piRNAs revealed experimentally validated and predicted mRNA targets expressed in the BSM cells. Thirty-eight of these mRNAs represent major targets for deregulated miRNAs and might play important roles in the pathophysiology of asthma. Interestingly, 6 of these mRNAs were previously associated with asthma, considered as novel therapeutic targets for treatment of this disease, or both. Signaling pathway analysis revealed involvement of 38 miRNA-targeted mRNAs in increased cell proliferation through phosphatase and tensin homolog and phosphoinositide 3-kinase/Akt signaling pathways., Conclusions: BSM cells of asthmatic patients are characterized by aberrant sncRNA expression that recapitulates multiple pathologic phenotypes of these cells., (Copyright © 2015 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Background: Bronchial hyperresponsiveness (BHR) and variation in glutathione S-transferase (GST) genes have been associated with asthma risk. The relationship of these two risk factors with adult onset asthma in the general population was investigated., Methods: GSTP1 Ile105Val single nucleotide polymorphism and GSTM1 and GSTT1 gene deletion polymorphisms were genotyped in the population-representative SAPALDIA cohort. BHR was assessed at baseline by methacholine challenge and defined as a fall of > or =20% in forced expiratory volume in 1 s. Independent effects of GST polymorphisms and BHR on new onset of asthma after 11 years of follow-up were estimated by multiple logistic regression analysis, adjusting for relevant baseline measures. Effect modification was assessed by including interaction terms in the model., Results: Among 4426 asthma-free participants at baseline, 14% had BHR. At follow-up, 3.3% reported new onset of physician-diagnosed asthma. BHR (p<0.001) and GSTP1 Ile105Val genotype (p = 0.005) were independently associated with incident asthma, but no association was seen for GSTT1 and GSTM1 gene deletion polymorphisms. Among subjects free of respiratory symptoms at baseline, the effect of BHR on the risk of physician-diagnosed asthma at follow-up was restricted to GSTP1 105 Ile/Ile carriers (OR 4.57, 95% CI 2.43 to 8.57 vs 1.40, 95% CI 0.58 to 3.39; p for interaction = 0.023)., Conclusions: If confirmed by independent studies, our results suggest that GSTP1 Ile105Val genotype strongly determines the progression of BHR to physician-diagnosed asthma in the general population.

Background: Bronchial hyperresponsiveness (BHR) is a common feature of asthma. However, BHR is also present in asymptomatic individuals and its clinical and prognostic significance is unclear. We hypothesised that BHR might play a role in the development of chronic obstructive pulmonary disease (COPD) as well as asthma., Methods: In 1991 respiratory symptoms and BHR to methacholine were evaluated in 7126 of the 9651 participants in the SAPALDIA cohort study. Eleven years later 5825 of these participants were re-evaluated, of whom 4852 performed spirometric tests. COPD was defined as an FEV1/FVC ratio of <0.70., Results: In 1991 17% of participants had BHR, of whom 51% were asymptomatic. Eleven years later the prevalence of asthma, wheeze, and shortness of breath in formerly asymptomatic subjects with or without BHR was, respectively, 5.7% v 2.0%, 8.3% v 3.4%, and 19.1% v 11.9% (all p<0.001). Similar differences were observed for chronic cough (5.9% v 2.3%; p = 0.002) and COPD (37.9% v 14.3%; p<0.001). BHR conferred an adjusted odds ratio (OR) of 2.9 (95% CI 1.8 to 4.5) for wheezing at follow up among asymptomatic participants. The adjusted OR for COPD was 4.5 (95% CI 3.3 to 6.0). Silent BHR was associated with a significantly accelerated decline in FEV1 by 12 (5-18), 11 (5-16), and 4 (2-8) ml/year in current smokers, former smokers and never smokers, respectively, at SAPALDIA 2., Conclusions: BHR is a risk factor for an accelerated decline in FEV1 and the development of asthma and COPD, irrespective of atopic status. Current smokers with BHR have a particularly high loss of FEV1.

Evidence-based national and international guidelines are largely aimed to guide in the diagnosis and treatment of asthma or COPD, but none addresses sufficiently mixed disease states of both disorders, which are ill-defined but very common in the daily routine clinic. This is a consensus report of a workshop on mixed disease. Asthma is characterized by a classical clinical history and physical exam, reversible airflow limitation and a high degree of bronchial hyperresponsiveness. In contrast, history (mostly smoker) and findings in typical COPD are different: COPD patients have little if any bronchial hyperresponsiveness and reversibility of the airflow limitation, respectively. However, beyond the full reversible airflow limitation which excludes COPD or mixed disease, none of these criteria are fully discriminatory. Patients with some of the characteristics of both diseases should be classified as mixed disease. A definitive diagnosis however, should only be assigned in a dynamic process. Once diagnosed the patient should be continuously re-evaluated according to the strength of the diagnosis, since the consequent treatment is important: COPD patients with asthmatic phenotype need early inhaled corticosteroids, even if their FEV1 > 50 %. Moreover, allergen avoidance can be indicated. On the other hand, asthma patients with COPD phenotype could benefit from anticholinergics or--if indicated--pulmonary rehabilitation. Mixed disease should be diagnosed as the coexistence of two distinct entities, i. e. asthma (allergic or intrinsic asthma, whichever is appropriate) and COPD.

Objectives: The Swiss Cohort Study on Air Pollution and Lung Diseases in Adults (SAPALDIA) was designed to investigate the health effects from long-term exposure to air pollution., Methods: The health assessment at recruitment (1991) and at the first reassessment (2001-3) consisted of an interview about respiratory health, occupational and other exposures, spirometry, a methacholine bronchial challenge test, end-expiratory carbon monoxide (CO) measurement and measurement for atopy. A bio bank for DNA and blood markers was established. Heart rate variability was measured using a 24-hour ECG (Holter) in a random sample of participants aged 50 years and older. Concentrations of nitrogen dioxide (NO2), sulphur dioxide (SO2), ozone (O3) and particulates in ambient air have been monitored in all study areas since 1991. Residential histories collected over the 11 year follow-up period coupled with GIS modelling will provide individual long-term air pollutant exposure estimates., Results: Of 9651 participants examined in 1991, 8715 could be traced for the cohort study and 283 died. Basic information about health status was obtained for 8047 individuals (86% of alive persons), 6 528 individuals (70%) agreed to the health examination and 5 973 subjects (62%) completed the entire protocol. Non-participants in the reassessment were on average younger than participants and more likely to have been smokers and to have reported respiratory symptoms in the first assessment. Average weight had increased by 5.5 kg in 11 years and 28% of smokers in 1991 had quit by the time of the reassessment.

B-cell isotype switching and the production of IgE is regulated by a variety of gene products through different mechanisms. A better understanding of these processes has the potential to identify markers of disease and new therapeutic targets. The aim of the study was to investigate human B-cell isotype control and IgE production in atopy and asthma with cDNA array technology. Eighteen atopic asthmatic, eight atopic nonasthmatic, and fourteen healthy control subjects were included. Peripheral blood mononuclear cells were separated by gradient centrifugation, mRNA was purified, and the reverse-transcribed probes were hybridized to cDNA membranes. Group differences were assessed with the Mann-Whitney U-test. Twenty-three of seventy-eight tested IgE-related genes had significantly altered expression in atopy and asthma compared with that in the healthy subjects. The differentially expressed genes include surface molecules involved in T- and B-cell interaction and activation, cytokines, intracellular signaling products, and transcription factors. In conclusion, both atopic nonasthmatic and atopic asthmatic individuals had activated proinflammatory pathways, a minimal requirement for B-cell isotype switching, and a clear net pro-IgE cytokine climate.

Bronchial asthma is a very common disease which often remains underdiagnosed. The aim of this study was to determine the predictive value of the most common respiratory symptoms and to explore the best symptom combinations to predict diagnosis of asthma. A questionnaire comprising common respiratory symptoms was submitted to 9,651 subjects aged 18-60 yrs, randomly selected from the Swiss population, of whom 225 subjects (2.3%) had current asthma as confirmed by their general practitioner. Based on these data the authors calculated the predictive values of single symptoms and symptom combinations to diagnose asthma. Wheezing was the most sensitive single symptom (sensitivity 75%). Simple symptoms such as wheezing with dyspnoea, chronic phlegm or chronic cough had specificity greater than 95%. Wheezing with dyspnoea (WD) or nocturnal dyspnoea (ND) had the best positive predictive value (PPV) as isolated symptoms (24% and 21%, respectively). When combining symptoms, wheezing associated with daily dyspnoea at rest or nocturnal dyspnoea showed the best PPV (42% and 39%, respectively), almost double single symptoms such as WD or ND. Wheezing associated with at least two of the three nocturnal symptoms (nocturnal dyspnoea, nocturnal cough or nocturnal chest tightness) had a sensitivity of 80% to diagnose asthma. In conclusion, respiratory symptoms obtained by medical history are reliable predictors of asthma. The findings suggest that particular combinations of symptoms are clinically useful in the differential diagnosis of asthma.

A variety of studies have stressed the importance of the control of inflammatory cell longevity and the balance of pro-survival and pro-apoptotic signalling. Recently, asthma was found to be associated with reduced apoptosis of inflammatory cells in lung tissue. The aim of the study was to investigate the systemic activation of apoptosis pathways using cDNA array technology in atopy and asthma. Eighteen atopic asthmatics (AA), eight atopic non-asthmatic (AN) and 14 healthy control subjects (C) were included in the study. Peripheral blood mononuclear cells were separated with gradient centrifugation, mRNA purified and the reverse-transcribed probes hybridized to cDNA arrays. The signals were compared by standardizing to the 100 most expressed genes and group differences assessed with the Mann-Whitney U-test. We found a concerted up-regulation of several pro-survival cytokines and growth factors in AN and AA. FAS and FASL were not differentially expressed, but FAST kinase was over-expressed in AN and AA. The tumour necrosis factor pathway was activated in AN and AA with increased cytokine and receptor levels and increased TRAF2, an intracellular signalling product. There were indications of a down-regulated p53 system. In contrast, the Bcl-2 family of genes showed a net pro-apoptotic profile in AN and AA. The group of caspases showed a constant gene expression pattern in all groups. In conclusion, significant differences in the expression of apoptosis-related genes were found in peripheral blood of atopic individuals with and without asthma. cDNA array technology proved to be useful and may be complementary to DNA-based studies in order to analyse interactive and multidimensional pathways as shown here for apoptosis.

Background: Inhaled corticosteroids are currently the cornerstone of asthma treatment. Some studies of high-dose fluticasone propionate in patients with no or mild asthma have, however, suggested substantial systemic absorption. We investigated the pharmacokinetics of fluticasone propionate in patients with asthma receiving appropriate doses for severity., Methods: We did a double-blind, randomised, crossover study in 11 patients with asthma and 13 matched healthy controls (age 20-65 years; asthma patients forced expiratory volume in 1 s <75% and stable on high-dose inhaled corticosteroids). Patients received one 1000 microg intravenous dose or 1000 microg daily for 7 days inhaled (via spacer device) fluticasone propionate. In the 12 h after dosing, we monitored plasma fluticasone propionate and cortisol concentrations by mass spectrometry and competitive immunoassay with use of direct chemiluminescence. Analysis was by intention to treat., Findings: After inhalation, geometric mean values were significantly lower in the asthma group than in controls for fluticasone propionate plasma area under curve (1082 [95% CI 850-1451] vs 2815 pg mL(-1) h(-1) [2262-3949], -62% difference [45-72]; p<0.001), maximum concentrations (117 [91-159] vs 383 pg/mL [302-546], -68% [-50 to -81]; p<0.001), and systemic bioavailability (10.1 [7.9-14.0] vs 21.4% [15.4-32.2], -54% [-27 to -70]; p=0.001). Intravenous-dose clearance, volume of distribution at steady state, plasma half-life, and mean residence time, were similar in the two groups. Less suppression of plasma cortisol concentrations was seen in the asthma group than in controls 4-12 h after inhaled fluticasone propionate., Interpretation: Systemic availability of fluticasone propionate is substantially less in patients with moderate to severe asthma than in healthy controls. Inhaled corticosteroids that are absorbed through the lungs need to be assessed in patients who are receiving doses appropriate for disease severity, and not in normal volunteers.

Background: Early exposure to dust mite allergens may be critical for primary sensitization. Reducing exposure may offer a realistic chance for primary prevention of sensitization and asthma, but it is essential to implement measures that can achieve and maintain the low-allergen environment., Objective: Our purpose was to assess the effectiveness of mite allergen avoidance measures in achieving and maintaining a low-allergen environment during pregnancy and in the first year of life., Methods: The Manchester Asthma and Allergy Study is a prospective, prenatally randomized study that follows the development of asthma and atopy in a cohort of infants at high risk (both parents atopic) who are randomly allocated to full mite allergen avoidance or to a normal regimen. Avoidance measures comprise (1) mite-proof covers (mattress, pillow, and quilt) for parental bed, (2) high-filtration vacuum cleaner, (3) vinyl flooring in infant's bedroom, (4) new crib and portable crib mattresses encased in mite-proof material, (5) benzyl benzoate (Acarosan) applied on carpets and soft furniture, (6) bed linens washed in hot water weekly, and (7) washable soft toys. Dust samples from the parental bed, bedroom floor, living room floor, infant's mattress, and nursery floor were collected between the 10th and 14th weeks of pregnancy, immediately after birth, and then at age 6 months and 1 year, and Der p 1 levels were determined by mAb-based ELISA., Results: Recovered Der p 1 from maternal mattress was reduced by 97. 25% (95% confidence interval [CI] 95.25%-98.41%) during the second and third trimesters of pregnancy, with the effect persisting for 6 months (98% reduction, 95% CI 97.25%-99.1%) and 12 months (97.6% reduction, 95% CI 95.7%-98.6%) after the birth (active vs control, P <.000001). Total Der p 1 from bedroom floor in the active group was reduced by 53.7% (95% CI 25.7%-71.2%) in samples collected within 4 weeks of the child's birth, with the percentage reduction being 62. 8% (95% CI 39.3%-77.2%) at 6 months and 26.5% (95% CI -24% to 57.1%) at 1 year (active compared vs control, P <.007). Der p 1 levels in crib mattress and nursery floor in the active group were extremely low (crib mattresses geometric mean [95% CI] 2.3 ng [1.6-3.4] at birth, 6.8 ng [4.5-10] at age 6 months, and 15.6 ng [9.8-24.8] at age 1 year [active vs control, P =.001]; nursery 1 ng [0.9-1.1] at birth, 1.7 ng [1.2-2.5] at age 6 months, and 2 ng [1.3-3.5] at age 1 year [active vs control, P <.00001]). The total amount of allergen recovered at age 1 year was 29-fold (95% CI 15.1- to 56.7-fold) higher in the control group than in the active group., Conclusions: The avoidance measures used in this study achieved and maintained a low mite allergen environment during pregnancy and in the first year of life in homes of infants at risk of atopy.

Total serum IgE, Phadiatop, and the skin prick test (SPT) are commonly used to diagnose atopic diseases. However, no large study has ever been done to test their diagnostic efficiency. We studied the diagnostic value of these three atopic markers in 8329 well-randomized adults from the Swiss Population Registry. The prevalence of current allergic asthma (CAA) was 1.8% and of current allergic rhinitis (CAR) 16.3%. The prevalences of positive Phadiatop, positive SPT (at least, one out of eight SPT to common aeroallergens with a wheal of > or = 3 mm), and positive total IgE (IgE > or = 100 kU/l) were 29, 23, and 23%, respectively. To diagnose CAA and CAR, the sensitivity of Phadiatop was significantly higher than that of SPT (72.5% vs 65.4%, 77.1% vs 68.4% respectively; P < 0.01 and < 0.001) and IgE (72.5% vs 56.9%, 77.1% vs 43.9%, respectively; both P < 0.001). The sensitivity of SPT was significantly higher (68.4% vs 43.9% P < 0.001) than that of IgE to diagnose CAR. When CAA and CAR were excluded, the SPT specificity was significantly higher than that of Phadiatop (77.8% vs 71.9% and 85.9% vs 80.5%, respectively; both P < 0.001): when CAR was excluded, SPT was significantly higher than IgE (85.9 vs 81.4%; P < 0.001). SPT had significantly the best positive predictive value for CAA (5.2% for SPT vs 4.6% for both IgE and Phadiatop; both P < 0.001) and CAR (48.7% for SPT vs 43.5% for Phadiatop and 31.6% for IgE; both P < 0.001). The three markers of atopy had roughly the same negative predictive value (NPV) for CAA, but IgE had a significantly lower NPV for CAR than SPT and Phadiatop (88.1% vs 93.3% and 94.7%, respectively; both P < 0.001). The diagnostic efficiency of SPT was significantly higher than that of Phadiatop (83.1% vs 79.9% and 77.6 vs 71.9%, respectively; both P < 0.001) to diagnose CAR and CAA. IgE and SPT had equal efficiency (77.6%), which was significantly higher than that of Phadiatop, to diagnose CAA (71.9%; both P < 0.001). In conclusion, SPT have the best positive predictive value and the best efficiency to diagnose respiratory atopic diseases. Furthermore, SPT give information on sensitivity to individual allergens and should therefore be used primarily by clinicians to assess respiratory allergic diseases. Moreover, they are cheaper and provide immediate, educational information for both patient and physician.

Background: Atopy and allergic phenotypes are biologically characterized by an imbalanced T helper cell response skewed towards a type 2 (TH2) immune response associated with elevated serum immunoglobulin E (IgE) levels. Polymorphisms in cytokine genes might modulate regulation of the TH1/TH2 balance. We thus aimed at reproducing our previous findings from a European study population on the association of various cytokine polymorphisms with self-reported hay fever as well as increased total and specific IgE levels in two comparable study populations. Methods: Two prospective Caucasian cohorts were used. In the Basel center of the European Community Respiratory Health Survey (ECRHS, n = 418) ten distinct cytokine polymorphisms of putative functional relevance were genotyped. In the Swiss cohort Study on Air Pollution And Lung Disease In Adults (SAPALDIA, n = 6003) two cytokine polymorphisms were genotyped. The associations of these polymorphisms with atopy were estimated by covariance and logistic regression analysis. Results: We confirmed IL4, IL10, IL6 and IL18 as candidate genes for atopic health outcomes. In the large, well-characterized SAPALDIA cohort the IL6(-174G>C) and IL18(-137G>C) polymorphisms were associated with circulating total IgE concentrations in subjects with hay fever. The IL18(-137G>C) polymorphism was also associated with the prevalence of hay fever. Conclusion: Comprehensive characterization of genetic variation in extended cytokine candidate gene regions is now needed. Large study networks must follow to investigate the association of risk patterns defined by genetic predisposing and environmental risk factors with specific atopic phenotypes. [ABSTRACT FROM AUTHOR]

We investigated the relationship between exercise-induced bronchospasm (EIB) and specific IgEs for seasonal (S-IgE) and perennial (P-IgE) allergens. The study, outside the main pollen season, was conducted on 289 20-year-old soldiers, who completed a self-administered questionnaire. A total of 289 subjects had S-IgE and P-IgE measured. The population was divided into subjects with (n = 166) and without (n = 123) history of atopic diseases (HAD). Twenty-three of 289 subjects (8%) had asthma, 70/289 (24%) allergic rhinitis, and 92/289 (32%) atopic siblings. Measured EIB was found in 17/289 subjects (6%). They had significantly higher levels of S-IgE and P-IgE than those without measured EIB (respectively, P< 0.01 and P< 0.05). The odds ratios of having EIB were significantly increased in the entire population in relationship with an increase in both S-IgE and P-IgE (chi-square test for trend = 9.4 and 12.7, P< 0.002 and 0.001, respectively). Interestingly, this highly significant relationship remained true when considering only the no HAD group (chi-square test = 7.4 and 8.8, P< 0.006 and 0.003, respectively). Outside the pollen season, EIB was highly related to the level of both specific seasonal and perennial IgEs in the total population and in the subjects without HAD. This suggests that even in young adults who have been asymptomatic throughout their life EIB appears to be closely linked to seasonal or perennial allergic diathesis as measured by specific IgEs. [ABSTRACT FROM AUTHOR]