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Abstract Rationale Occupational exposures can contribute to the exacerbation as well as the onset of asthma. However, work-exacerbated asthma (WEA) has received less attention than occupational asthma (OA) that is caused by work. Objectives The purpose of this Statement is to summarize current knowledge about the descriptive epidemiology, clinical characteristics, and management and treatment of WEA; propose a case definition for WEA; and discuss needs for prevention and research. Methods Information about WEA was identified primarily by systematic searches of the medical literature. Statements about prevention and research needs were reached by consensus. Measurements and Main Results WEA is defined as the worsening of asthma due to conditions at work. WEA is common, with a median prevalence of 21.5% among adults with asthma. Different types of agents or conditions at work may exacerbate asthma. WEA cases with persistent work-related symptoms can have clinical characteristics (level of severity, medication needs) and adverse socioeconomic outcomes (unemployment, reduction in income) similar to those of OA cases. Compared with adults with asthma unrelated to work, WEA cases report more days with symptoms, seek more medical care, and have a lower quality of life. WEA should be considered in any patient with asthma that is getting worse or who has work-related symptoms. Management of WEA should focus on reducing work exposures and optimizing standard medical management, with a change in jobs only if these measures are not successful. Conclusions WEA is a common and underrecognized adverse outcome resulting from conditions at work. Additional research is needed to improve the understanding of the risk factors for, and mechanisms and outcomes of, WEA, and to inform and evaluate preventive interventions.

The present document is the result of a consensus reached by a panel of experts from European and non-European countries on Occupational Rhinitis (OR), a disease of emerging relevance which has received little attention in comparison to occupational asthma. The document covers the main items of OR including epidemiology, diagnosis, management, socio-economic impact, preventive strategies and medicolegal issues. An operational definition and classification of OR tailored on that of occupational asthma, as well as a diagnostic algorithm based on steps allowing for different levels of diagnostic evidence are proposed. The needs for future research are pointed out. Key messages are issued for each item.

Background: Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) play a role in the pathogenesis of asthma. MMP-9 increases in the sputum of asthmatic patients after bronchial challenge with common allergens. We sought to assess whether a high-molecular-weight occupational allergen was able to induce changes in MMP-9 as well as in other MMPs and TIMPs in subjects with occupational asthma. Methods: Ten patients underwent specific inhalation challenge (SIC) on 2 consecutive days. We monitored changes in lung function by measuring FEV 1 for 7 h. Induced sputum test was performed at 6 h after sham and flour challenge. The total and differential cell counts were analyzed. Levels of MMPs (specifically MMP-2, MMP-7, MMP-9 and MMP-13) were measured using Fluorokine® MultiAnalyte Profiling kits and a Luminex® Bioanalyzer, while levels of TIMP-1 and TIMP-2 were measured by ELISA. Results: Flour challenge increased the percentage of eosinophils in sputum samples. Asthmatic reactions induced by flour were associated with a significant increase in the sputum level of MMP-9 (p = 0.05), but not in the levels of MMP-2, MMP-7, MMP-13, TIMP-1 and TIMP-2. Sputum levels of MMP-9 measured after flour challenge were nearly significantly correlated (r = 0.67; p = 0.06) with the maximal fall in FEV 1 observed during the asthmatic reaction, but they did not correlate with the number of neutrophils (r = 0.18; p = 0.7) and eosinophils (r = 0.55; p = 0.2). Conclusions: This study showed that MMP-9 increases in sputum samples from sensitized occupational asthma patients after SIC with flour.

Purpose of ReviewNumerous clinically relevant allergenic molecules enhance the performance of specific (s) IgE tests and improve the specificity of allergy diagnosis. This review aimed to summarize our current knowledge of the high-molecular-weight allergens involved in the development of occupational asthma and rhinitis and to critically analyze the contribution of component-resolved diagnosis in the management of these conditions.Recent FindingsThere is a lack of standardization and validation for most available extracts of occupational agents, and assessment of sIgE reactivity to occupational allergen components has been poorly investigated, with the notable exception of natural rubber latex (NRL) and wheat flour. In the case of NRL, the application of recombinant single allergens and amplification of natural extracts with stable recombinant allergens improved the test sensitivity. IgE-sensitization profile in patients with baker’s asthma showed great interindividual variation, and extract-based diagnostic is still recommended. For other occupational allergens, it remains necessary to evaluate the relevance of single allergen molecules for the sensitization induced by occupational exposure.SummaryProgress has been made to characterize occupational allergens especially NRL and wheat, although there is still an unmet need to increase the knowledge of occupational allergens, to include standardized tools into routine diagnostic, and to evaluate their usefulness in clinical practice.

Accumulating evidence indicates that the workplace environment substantially contributes to the global burden of asthma and rhinitis. Work-related asthma and rhinitis represent a public health concern due to their health and socioeconomic impacts. This article summarizes the scientific evidence on sensitizer-induced occupational asthma and rhinitis that has been published during the past 5 years. The review addresses the strategies for diagnosing and managing these highly prevalent occupational diseases.

To assess the frequency of cysticfibrosis transmembrane conductance regulator (CFTR) gene mutations inpatients with allergic bronchopulmonary aspergillosis (ABPA). Case-control study. All subjects in the study werescreened for the presence of 13 mutations in the CFTR gene (R117H,621 + 1G->T, R334 W, ΔF508, ΔI507, 1717–1G->A, G542X, R553X, G551D, R1162X, 3849 + 10kbC->T, W1282X, and N1303K). Moreover, theywere also screened for the presence of the 5T variant in intron 8. University hospital and community-basedhospital. Twenty-one white patients with ABPA participated in the study. The presence of CFTR mutations was alsoinvestigated in 43 white subjects with allergic asthma who did not showsensitization to Aspergillus fumigatus and in 142subjects seeking genetic counseling for diseases other than cysticfibrosis (CF). Six patients with ABPA werefound to be heterozygous for one CFTR mutation, including ΔF508(n = 2), G542X (n = 1), R1162X (n = 1), 1717–1G->A (n = 1),and R117H (n = 1). The 5T allele was not detected in ABPA patients. None of the ABPA patients showed sweat chloride concentrations > 60mEq/L. The frequency of CFTR mutation carriers was significantly higherin ABPA patients (6 of 21 patients; 28.5%) than in control asthmaticsubjects (2 of 43 subjects; 4.6%; p = 0.01) and in subjects seekinggenetic counseling (6 of 142 subjects; p < 0.001). These findings indicate that in patientswith out a clinical diagnosis of CF, CFTR gene mutations could beinvolved in the development of ABPA, in association with other geneticor environmental factors.

Work-related asthma (WRA) accounts for 10-15% of adult asthma. This review will summarize the available information related to the socioeconomic outcomes inherent to WRA. A substantial proportion of subjects suffering from WRA experience prolonged work disruption and subsequent loss of income. Moreover, recent studies have established that WRA is associated with a higher use of healthcare resources and a lower quality of life than asthma unrelated to work. The negative socioeconomic consequences are mostly influenced by professional and demographic factors, including reduced possibilities for relocation to an unexposed job within the same company, lack of effective retraining programs and low level of education. These socioeconomic considerations should be regarded as a central component in the implementation of rational management and prevention policies.

BackgroundThe natural history of asthma includes in some patients periods of disease remission, but the underlying mechanisms are unknown.ObjectivesWe explored whether type 1 myeloid dendritic cell (mDC) dysfunction could be involved in the persistence of asthma, studying the controlled setting of occupational asthma after allergen avoidance.MethodsWe recruited 32 patients with occupational asthma to flour or latex ascertained by specific inhalation challenge and who were no longer exposed to the causal allergen. Leukapheresis was performed in each patient to isolate and characterise blood type 1 mDCs, and their functionality was studied in coculture with allogeneic CD4+ T cells from controls.ResultsAt follow-up, 11/32 patients (34%) were characterised by the absence of symptoms and non-specific bronchial hyper-responsiveness to histamine and were considered to be cured. When compared with cured patients, mDCs from patients with persistent disease increased the production of interleukin (IL) 5 and IL-13 by CD4+ T cells, and upregulated programmed death ligand 2 (PD-L2) upon allergen pulsing. In addition, IL-5 and IL-13 responses could be reversed by exogenous IL-12, as well as by PD-L2 blockade.ConclusionsThis study indicates that pro-Th2 features of mDCs correlate with disease activity in asthma after cessation of exposure to the causal allergen. The findings also highlight that the Th2 programming by dendritic cells is flexible and partly mediated by PD-L2.